Protective effect of rhGLP-1 (7–36) on brain ischemia/reperfusion damage in diabetic rats
In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The pre...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Zhao, Libo [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015transfer abstract |
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| Schlagwörter: |
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| Umfang: |
7 |
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| Übergeordnetes Werk: |
Enthalten in: DNA methylation mediates gonadal development via regulating the expression levels of - Su, Junxiao ELSEVIER, 2023, an international multidisciplinary journal devoted to fundamental research in the brain sciences, Amsterdam |
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| Übergeordnetes Werk: |
volume:1602 ; year:2015 ; day:30 ; month:03 ; pages:153-159 ; extent:7 |
| Links: |
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| DOI / URN: |
10.1016/j.brainres.2015.01.014 |
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ELV034888578 |
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| 245 | 1 | 0 | |a Protective effect of rhGLP-1 (7–36) on brain ischemia/reperfusion damage in diabetic rats |
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| 520 | |a In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. | ||
| 520 | |a In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. | ||
| 650 | 7 | |a Diabetic rats |2 Elsevier | |
| 650 | 7 | |a Oxidative stress |2 Elsevier | |
| 650 | 7 | |a GLP-1 |2 Elsevier | |
| 650 | 7 | |a Brain ischemia/reperfusion |2 Elsevier | |
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| 700 | 1 | |a Wang, Qian |4 oth | |
| 700 | 1 | |a Qian, Zhonglian |4 oth | |
| 700 | 1 | |a Feng, Wanyu |4 oth | |
| 700 | 1 | |a Yin, Xiaoxing |4 oth | |
| 700 | 1 | |a Fang, Yi |4 oth | |
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10.1016/j.brainres.2015.01.014 doi GBVA2015020000029.pica (DE-627)ELV034888578 (ELSEVIER)S0006-8993(15)00025-6 DE-627 ger DE-627 rakwb eng 150 610 150 DE-600 610 DE-600 540 570 VZ BIODIV DE-30 fid 35.80 bkl 58.30 bkl Zhao, Libo verfasserin aut Protective effect of rhGLP-1 (7–36) on brain ischemia/reperfusion damage in diabetic rats 2015transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. Diabetic rats Elsevier Oxidative stress Elsevier GLP-1 Elsevier Brain ischemia/reperfusion Elsevier Xu, Jia oth Wang, Qian oth Qian, Zhonglian oth Feng, Wanyu oth Yin, Xiaoxing oth Fang, Yi oth Enthalten in Elsevier Su, Junxiao ELSEVIER DNA methylation mediates gonadal development via regulating the expression levels of 2023 an international multidisciplinary journal devoted to fundamental research in the brain sciences Amsterdam (DE-627)ELV010071113 volume:1602 year:2015 day:30 month:03 pages:153-159 extent:7 https://doi.org/10.1016/j.brainres.2015.01.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 35.80 Makromolekulare Chemie VZ 58.30 Biotechnologie VZ AR 1602 2015 30 0330 153-159 7 045F 150 |
| spelling |
10.1016/j.brainres.2015.01.014 doi GBVA2015020000029.pica (DE-627)ELV034888578 (ELSEVIER)S0006-8993(15)00025-6 DE-627 ger DE-627 rakwb eng 150 610 150 DE-600 610 DE-600 540 570 VZ BIODIV DE-30 fid 35.80 bkl 58.30 bkl Zhao, Libo verfasserin aut Protective effect of rhGLP-1 (7–36) on brain ischemia/reperfusion damage in diabetic rats 2015transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. Diabetic rats Elsevier Oxidative stress Elsevier GLP-1 Elsevier Brain ischemia/reperfusion Elsevier Xu, Jia oth Wang, Qian oth Qian, Zhonglian oth Feng, Wanyu oth Yin, Xiaoxing oth Fang, Yi oth Enthalten in Elsevier Su, Junxiao ELSEVIER DNA methylation mediates gonadal development via regulating the expression levels of 2023 an international multidisciplinary journal devoted to fundamental research in the brain sciences Amsterdam (DE-627)ELV010071113 volume:1602 year:2015 day:30 month:03 pages:153-159 extent:7 https://doi.org/10.1016/j.brainres.2015.01.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 35.80 Makromolekulare Chemie VZ 58.30 Biotechnologie VZ AR 1602 2015 30 0330 153-159 7 045F 150 |
| allfields_unstemmed |
10.1016/j.brainres.2015.01.014 doi GBVA2015020000029.pica (DE-627)ELV034888578 (ELSEVIER)S0006-8993(15)00025-6 DE-627 ger DE-627 rakwb eng 150 610 150 DE-600 610 DE-600 540 570 VZ BIODIV DE-30 fid 35.80 bkl 58.30 bkl Zhao, Libo verfasserin aut Protective effect of rhGLP-1 (7–36) on brain ischemia/reperfusion damage in diabetic rats 2015transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. Diabetic rats Elsevier Oxidative stress Elsevier GLP-1 Elsevier Brain ischemia/reperfusion Elsevier Xu, Jia oth Wang, Qian oth Qian, Zhonglian oth Feng, Wanyu oth Yin, Xiaoxing oth Fang, Yi oth Enthalten in Elsevier Su, Junxiao ELSEVIER DNA methylation mediates gonadal development via regulating the expression levels of 2023 an international multidisciplinary journal devoted to fundamental research in the brain sciences Amsterdam (DE-627)ELV010071113 volume:1602 year:2015 day:30 month:03 pages:153-159 extent:7 https://doi.org/10.1016/j.brainres.2015.01.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 35.80 Makromolekulare Chemie VZ 58.30 Biotechnologie VZ AR 1602 2015 30 0330 153-159 7 045F 150 |
| allfieldsGer |
10.1016/j.brainres.2015.01.014 doi GBVA2015020000029.pica (DE-627)ELV034888578 (ELSEVIER)S0006-8993(15)00025-6 DE-627 ger DE-627 rakwb eng 150 610 150 DE-600 610 DE-600 540 570 VZ BIODIV DE-30 fid 35.80 bkl 58.30 bkl Zhao, Libo verfasserin aut Protective effect of rhGLP-1 (7–36) on brain ischemia/reperfusion damage in diabetic rats 2015transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. Diabetic rats Elsevier Oxidative stress Elsevier GLP-1 Elsevier Brain ischemia/reperfusion Elsevier Xu, Jia oth Wang, Qian oth Qian, Zhonglian oth Feng, Wanyu oth Yin, Xiaoxing oth Fang, Yi oth Enthalten in Elsevier Su, Junxiao ELSEVIER DNA methylation mediates gonadal development via regulating the expression levels of 2023 an international multidisciplinary journal devoted to fundamental research in the brain sciences Amsterdam (DE-627)ELV010071113 volume:1602 year:2015 day:30 month:03 pages:153-159 extent:7 https://doi.org/10.1016/j.brainres.2015.01.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 35.80 Makromolekulare Chemie VZ 58.30 Biotechnologie VZ AR 1602 2015 30 0330 153-159 7 045F 150 |
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10.1016/j.brainres.2015.01.014 doi GBVA2015020000029.pica (DE-627)ELV034888578 (ELSEVIER)S0006-8993(15)00025-6 DE-627 ger DE-627 rakwb eng 150 610 150 DE-600 610 DE-600 540 570 VZ BIODIV DE-30 fid 35.80 bkl 58.30 bkl Zhao, Libo verfasserin aut Protective effect of rhGLP-1 (7–36) on brain ischemia/reperfusion damage in diabetic rats 2015transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. Diabetic rats Elsevier Oxidative stress Elsevier GLP-1 Elsevier Brain ischemia/reperfusion Elsevier Xu, Jia oth Wang, Qian oth Qian, Zhonglian oth Feng, Wanyu oth Yin, Xiaoxing oth Fang, Yi oth Enthalten in Elsevier Su, Junxiao ELSEVIER DNA methylation mediates gonadal development via regulating the expression levels of 2023 an international multidisciplinary journal devoted to fundamental research in the brain sciences Amsterdam (DE-627)ELV010071113 volume:1602 year:2015 day:30 month:03 pages:153-159 extent:7 https://doi.org/10.1016/j.brainres.2015.01.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 35.80 Makromolekulare Chemie VZ 58.30 Biotechnologie VZ AR 1602 2015 30 0330 153-159 7 045F 150 |
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Protective effect of rhGLP-1 (7–36) on brain ischemia/reperfusion damage in diabetic rats |
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In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. |
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In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. |
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In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV034888578</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625202235.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2015 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.brainres.2015.01.014</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2015020000029.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV034888578</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0006-8993(15)00025-6</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">150</subfield><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">150</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">540</subfield><subfield code="a">570</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">BIODIV</subfield><subfield code="q">DE-30</subfield><subfield code="2">fid</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">35.80</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">58.30</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Zhao, Libo</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Protective effect of rhGLP-1 (7–36) on brain ischemia/reperfusion damage in diabetic rats</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2015transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">7</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">In recent years, GLP-1 and its analogs have been developed for the treatment of type 2 diabetes. It has been reported that stimulating the GLP-1 receptor can protect neurons against metabolic and oxidative insults, and therefore can be used in the treatment of stroke and Parkinson׳s disease. The present study aimed to examine the neuroprotective effects of rhGLP-1 (7–36) and its possible mechanisms against acute ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in diabetic rats. The type 2 diabetic rat model was established by a combination of a high-fat diet and low-dose streptozotocin (STZ). RhGLP-1 (7–36) (20, 40, 80μg/kg) was given intraperitoneally before reperfusion. The neuroprotective effects of rhGLP-1 (7–36) were evaluated by changes in neurological deficit scores and 2,3,5-Triphenyltetrazolium chloride (TTC) staining. Changes in blood glucose were used to assess hypoglycemic effects. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide syntheses (iNOS) and endothelial nitric oxide syntheses (eNOS) after MCAO/R administration (2h and 46h) were examined to investigate the possible mechanisms of RhGLP-1 (7–36). Haematoxylin and eosin (H&E) staining was used for histopathological observation. Compared with the control group, rhGLP-1 (7–36)-treated groups decreased nerve function deficiency scores; significantly reduced infarction volume percentage, MDA, iNOS and blood glucose; and significantly increased SOD, GSH-PX and eNOS. In addition, rhGLP-1 (7–36) groups enhanced the density of surviving neurons and increased vascular proliferation. The current study suggests a neuroprotective effect of rhGLP-1 (7–36) in diabetic MCAO/R rats since anti-oxidative and anti-nitrosative stress effects can contribute to beneficial effects against ischemia/reperfusion injury.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Diabetic rats</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Oxidative stress</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">GLP-1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Brain ischemia/reperfusion</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xu, Jia</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Qian</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Qian, Zhonglian</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Feng, Wanyu</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yin, Xiaoxing</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Fang, Yi</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Su, Junxiao ELSEVIER</subfield><subfield code="t">DNA methylation mediates gonadal development via regulating the expression levels of</subfield><subfield code="d">2023</subfield><subfield code="d">an international multidisciplinary journal devoted to fundamental research in the brain sciences</subfield><subfield code="g">Amsterdam</subfield><subfield code="w">(DE-627)ELV010071113</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:1602</subfield><subfield code="g">year:2015</subfield><subfield code="g">day:30</subfield><subfield code="g">month:03</subfield><subfield code="g">pages:153-159</subfield><subfield code="g">extent:7</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.brainres.2015.01.014</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">FID-BIODIV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">35.80</subfield><subfield code="j">Makromolekulare Chemie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">58.30</subfield><subfield code="j">Biotechnologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">1602</subfield><subfield code="j">2015</subfield><subfield code="b">30</subfield><subfield code="c">0330</subfield><subfield code="h">153-159</subfield><subfield code="g">7</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">150</subfield></datafield></record></collection>
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