Ginsenoside Rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury

Ginsenoside Rg1 (GS Rg1) is a glycosylated triterpenoid saponin extracted from Panax ginseng. We aim to investigate the impact of GS Rg1 on protein aggregation and inflammatory response in a cerebral ischemia/reperfusion (I/R) injury model. Rats were administered different doses of GS Rg1 (10, 20, o...
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Gespeichert in:

Autor*in:	Zheng, Tianyang [verfasserIn] Jiang, Hong [verfasserIn] Jin, Rihua [verfasserIn] Zhao, Yiming [verfasserIn] Bai, Yang [verfasserIn] Xu, Haiyang [verfasserIn] Chen, Yong [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	Ginsenoside Rg1 Stroke Ubiquitinated aggregates Inflammatory response Proteasome

Übergeordnetes Werk:	Enthalten in: European journal of pharmacology - New York, NY [u.a.] : Elsevier, 1967, 853, Seite 65-73
Übergeordnetes Werk:	volume:853 ; pages:65-73

DOI / URN:	10.1016/j.ejphar.2019.02.018

Katalog-ID:	ELV00217507X

Internformat


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245	1	0	\|a Ginsenoside Rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury
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520			\|a Ginsenoside Rg1 (GS Rg1) is a glycosylated triterpenoid saponin extracted from Panax ginseng. We aim to investigate the impact of GS Rg1 on protein aggregation and inflammatory response in a cerebral ischemia/reperfusion (I/R) injury model. Rats were administered different doses of GS Rg1 (10, 20, or 40 mg/kg/day) or nimodipine (1 mg/kg/day) for 5 consecutive days. Cerebral I/R injury was induced by middle cerebral artery occlusion for 2 h followed by a 22 h reperfusion period. Next, we examined the differences in infarct volume and neurological deficit via TTC staining and Longa′s scoring, respectively. Furthermore, the differences in protein aggregates, proteasome, IκBα and NF-κB in the cerebral cortices were investigated through western blotting. The distribution of ubiquitin, proteasome and NF-κB in the neocortex were examined through immunohistochemistry. Pro-inflammatory cytokines were measured using ELISA and proteasome activity was determined by fluorometric peptidaseassay. Treatment with GS Rg1 40 mg/kg resulted in a significantly lower infarct volume and improved the neurological deficit score as well as the histological appearance compared to the control I/R group (P < 0.05). GS Rg1 treatment resulted in significantly lower proinflammatory cytokine expressions and suppression of the nuclear translocation of NF-κB as well as the phosphorylation of IκBα (P < 0.01). Finally, GS Rg1 treatment decreased the proteasomal activity and protein aggregate accumulation in brain tissues (P < 0.01). Our results confirm the neuroprotective function of GS Rg1 at 40 mg/kg. This effect may be attributed to a decrease in ubiquitinated aggregates and a suppression of the inflammatory response after I/R insult.
650		4	\|a Ginsenoside Rg1
650		4	\|a Stroke
650		4	\|a Ubiquitinated aggregates
650		4	\|a Inflammatory response
650		4	\|a Proteasome
700	1		\|a Jiang, Hong \|e verfasserin \|4 aut
700	1		\|a Jin, Rihua \|e verfasserin \|4 aut
700	1		\|a Zhao, Yiming \|e verfasserin \|4 aut
700	1		\|a Bai, Yang \|e verfasserin \|4 aut
700	1		\|a Xu, Haiyang \|e verfasserin \|4 aut
700	1		\|a Chen, Yong \|e verfasserin \|4 aut
773	0	8	\|i Enthalten in \|t European journal of pharmacology \|d New York, NY [u.a.] : Elsevier, 1967 \|g 853, Seite 65-73 \|h Online-Ressource \|w (DE-627)300897340 \|w (DE-600)1483526-5 \|w (DE-576)081952627 \|x 1879-0712 \|7 nnns
773	1	8	\|g volume:853 \|g pages:65-73
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912			\|a GBV_ILN_4305
912			\|a GBV_ILN_4313
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912			\|a GBV_ILN_4335
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4393
936	b	k	\|a 44.38 \|j Pharmakologie
951			\|a AR
952			\|d 853 \|h 65-73

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publishDate	2019
allfields	10.1016/j.ejphar.2019.02.018 doi (DE-627)ELV00217507X (ELSEVIER)S0014-2999(19)30112-8 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Zheng, Tianyang verfasserin aut Ginsenoside Rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Ginsenoside Rg1 (GS Rg1) is a glycosylated triterpenoid saponin extracted from Panax ginseng. We aim to investigate the impact of GS Rg1 on protein aggregation and inflammatory response in a cerebral ischemia/reperfusion (I/R) injury model. Rats were administered different doses of GS Rg1 (10, 20, or 40 mg/kg/day) or nimodipine (1 mg/kg/day) for 5 consecutive days. Cerebral I/R injury was induced by middle cerebral artery occlusion for 2 h followed by a 22 h reperfusion period. Next, we examined the differences in infarct volume and neurological deficit via TTC staining and Longa′s scoring, respectively. Furthermore, the differences in protein aggregates, proteasome, IκBα and NF-κB in the cerebral cortices were investigated through western blotting. The distribution of ubiquitin, proteasome and NF-κB in the neocortex were examined through immunohistochemistry. Pro-inflammatory cytokines were measured using ELISA and proteasome activity was determined by fluorometric peptidaseassay. Treatment with GS Rg1 40 mg/kg resulted in a significantly lower infarct volume and improved the neurological deficit score as well as the histological appearance compared to the control I/R group (P < 0.05). GS Rg1 treatment resulted in significantly lower proinflammatory cytokine expressions and suppression of the nuclear translocation of NF-κB as well as the phosphorylation of IκBα (P < 0.01). Finally, GS Rg1 treatment decreased the proteasomal activity and protein aggregate accumulation in brain tissues (P < 0.01). Our results confirm the neuroprotective function of GS Rg1 at 40 mg/kg. This effect may be attributed to a decrease in ubiquitinated aggregates and a suppression of the inflammatory response after I/R insult. Ginsenoside Rg1 Stroke Ubiquitinated aggregates Inflammatory response Proteasome Jiang, Hong verfasserin aut Jin, Rihua verfasserin aut Zhao, Yiming verfasserin aut Bai, Yang verfasserin aut Xu, Haiyang verfasserin aut Chen, Yong verfasserin aut Enthalten in European journal of pharmacology New York, NY [u.a.] : Elsevier, 1967 853, Seite 65-73 Online-Ressource (DE-627)300897340 (DE-600)1483526-5 (DE-576)081952627 1879-0712 nnns volume:853 pages:65-73 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 853 65-73
spelling	10.1016/j.ejphar.2019.02.018 doi (DE-627)ELV00217507X (ELSEVIER)S0014-2999(19)30112-8 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Zheng, Tianyang verfasserin aut Ginsenoside Rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Ginsenoside Rg1 (GS Rg1) is a glycosylated triterpenoid saponin extracted from Panax ginseng. We aim to investigate the impact of GS Rg1 on protein aggregation and inflammatory response in a cerebral ischemia/reperfusion (I/R) injury model. Rats were administered different doses of GS Rg1 (10, 20, or 40 mg/kg/day) or nimodipine (1 mg/kg/day) for 5 consecutive days. Cerebral I/R injury was induced by middle cerebral artery occlusion for 2 h followed by a 22 h reperfusion period. Next, we examined the differences in infarct volume and neurological deficit via TTC staining and Longa′s scoring, respectively. Furthermore, the differences in protein aggregates, proteasome, IκBα and NF-κB in the cerebral cortices were investigated through western blotting. The distribution of ubiquitin, proteasome and NF-κB in the neocortex were examined through immunohistochemistry. Pro-inflammatory cytokines were measured using ELISA and proteasome activity was determined by fluorometric peptidaseassay. Treatment with GS Rg1 40 mg/kg resulted in a significantly lower infarct volume and improved the neurological deficit score as well as the histological appearance compared to the control I/R group (P < 0.05). GS Rg1 treatment resulted in significantly lower proinflammatory cytokine expressions and suppression of the nuclear translocation of NF-κB as well as the phosphorylation of IκBα (P < 0.01). Finally, GS Rg1 treatment decreased the proteasomal activity and protein aggregate accumulation in brain tissues (P < 0.01). Our results confirm the neuroprotective function of GS Rg1 at 40 mg/kg. This effect may be attributed to a decrease in ubiquitinated aggregates and a suppression of the inflammatory response after I/R insult. Ginsenoside Rg1 Stroke Ubiquitinated aggregates Inflammatory response Proteasome Jiang, Hong verfasserin aut Jin, Rihua verfasserin aut Zhao, Yiming verfasserin aut Bai, Yang verfasserin aut Xu, Haiyang verfasserin aut Chen, Yong verfasserin aut Enthalten in European journal of pharmacology New York, NY [u.a.] : Elsevier, 1967 853, Seite 65-73 Online-Ressource (DE-627)300897340 (DE-600)1483526-5 (DE-576)081952627 1879-0712 nnns volume:853 pages:65-73 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 853 65-73
allfields_unstemmed	10.1016/j.ejphar.2019.02.018 doi (DE-627)ELV00217507X (ELSEVIER)S0014-2999(19)30112-8 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Zheng, Tianyang verfasserin aut Ginsenoside Rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Ginsenoside Rg1 (GS Rg1) is a glycosylated triterpenoid saponin extracted from Panax ginseng. We aim to investigate the impact of GS Rg1 on protein aggregation and inflammatory response in a cerebral ischemia/reperfusion (I/R) injury model. Rats were administered different doses of GS Rg1 (10, 20, or 40 mg/kg/day) or nimodipine (1 mg/kg/day) for 5 consecutive days. Cerebral I/R injury was induced by middle cerebral artery occlusion for 2 h followed by a 22 h reperfusion period. Next, we examined the differences in infarct volume and neurological deficit via TTC staining and Longa′s scoring, respectively. Furthermore, the differences in protein aggregates, proteasome, IκBα and NF-κB in the cerebral cortices were investigated through western blotting. The distribution of ubiquitin, proteasome and NF-κB in the neocortex were examined through immunohistochemistry. Pro-inflammatory cytokines were measured using ELISA and proteasome activity was determined by fluorometric peptidaseassay. Treatment with GS Rg1 40 mg/kg resulted in a significantly lower infarct volume and improved the neurological deficit score as well as the histological appearance compared to the control I/R group (P < 0.05). GS Rg1 treatment resulted in significantly lower proinflammatory cytokine expressions and suppression of the nuclear translocation of NF-κB as well as the phosphorylation of IκBα (P < 0.01). Finally, GS Rg1 treatment decreased the proteasomal activity and protein aggregate accumulation in brain tissues (P < 0.01). Our results confirm the neuroprotective function of GS Rg1 at 40 mg/kg. This effect may be attributed to a decrease in ubiquitinated aggregates and a suppression of the inflammatory response after I/R insult. Ginsenoside Rg1 Stroke Ubiquitinated aggregates Inflammatory response Proteasome Jiang, Hong verfasserin aut Jin, Rihua verfasserin aut Zhao, Yiming verfasserin aut Bai, Yang verfasserin aut Xu, Haiyang verfasserin aut Chen, Yong verfasserin aut Enthalten in European journal of pharmacology New York, NY [u.a.] : Elsevier, 1967 853, Seite 65-73 Online-Ressource (DE-627)300897340 (DE-600)1483526-5 (DE-576)081952627 1879-0712 nnns volume:853 pages:65-73 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 853 65-73
allfieldsGer	10.1016/j.ejphar.2019.02.018 doi (DE-627)ELV00217507X (ELSEVIER)S0014-2999(19)30112-8 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Zheng, Tianyang verfasserin aut Ginsenoside Rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Ginsenoside Rg1 (GS Rg1) is a glycosylated triterpenoid saponin extracted from Panax ginseng. We aim to investigate the impact of GS Rg1 on protein aggregation and inflammatory response in a cerebral ischemia/reperfusion (I/R) injury model. Rats were administered different doses of GS Rg1 (10, 20, or 40 mg/kg/day) or nimodipine (1 mg/kg/day) for 5 consecutive days. Cerebral I/R injury was induced by middle cerebral artery occlusion for 2 h followed by a 22 h reperfusion period. Next, we examined the differences in infarct volume and neurological deficit via TTC staining and Longa′s scoring, respectively. Furthermore, the differences in protein aggregates, proteasome, IκBα and NF-κB in the cerebral cortices were investigated through western blotting. The distribution of ubiquitin, proteasome and NF-κB in the neocortex were examined through immunohistochemistry. Pro-inflammatory cytokines were measured using ELISA and proteasome activity was determined by fluorometric peptidaseassay. Treatment with GS Rg1 40 mg/kg resulted in a significantly lower infarct volume and improved the neurological deficit score as well as the histological appearance compared to the control I/R group (P < 0.05). GS Rg1 treatment resulted in significantly lower proinflammatory cytokine expressions and suppression of the nuclear translocation of NF-κB as well as the phosphorylation of IκBα (P < 0.01). Finally, GS Rg1 treatment decreased the proteasomal activity and protein aggregate accumulation in brain tissues (P < 0.01). Our results confirm the neuroprotective function of GS Rg1 at 40 mg/kg. This effect may be attributed to a decrease in ubiquitinated aggregates and a suppression of the inflammatory response after I/R insult. Ginsenoside Rg1 Stroke Ubiquitinated aggregates Inflammatory response Proteasome Jiang, Hong verfasserin aut Jin, Rihua verfasserin aut Zhao, Yiming verfasserin aut Bai, Yang verfasserin aut Xu, Haiyang verfasserin aut Chen, Yong verfasserin aut Enthalten in European journal of pharmacology New York, NY [u.a.] : Elsevier, 1967 853, Seite 65-73 Online-Ressource (DE-627)300897340 (DE-600)1483526-5 (DE-576)081952627 1879-0712 nnns volume:853 pages:65-73 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 853 65-73
allfieldsSound	10.1016/j.ejphar.2019.02.018 doi (DE-627)ELV00217507X (ELSEVIER)S0014-2999(19)30112-8 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Zheng, Tianyang verfasserin aut Ginsenoside Rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Ginsenoside Rg1 (GS Rg1) is a glycosylated triterpenoid saponin extracted from Panax ginseng. We aim to investigate the impact of GS Rg1 on protein aggregation and inflammatory response in a cerebral ischemia/reperfusion (I/R) injury model. Rats were administered different doses of GS Rg1 (10, 20, or 40 mg/kg/day) or nimodipine (1 mg/kg/day) for 5 consecutive days. Cerebral I/R injury was induced by middle cerebral artery occlusion for 2 h followed by a 22 h reperfusion period. Next, we examined the differences in infarct volume and neurological deficit via TTC staining and Longa′s scoring, respectively. Furthermore, the differences in protein aggregates, proteasome, IκBα and NF-κB in the cerebral cortices were investigated through western blotting. The distribution of ubiquitin, proteasome and NF-κB in the neocortex were examined through immunohistochemistry. Pro-inflammatory cytokines were measured using ELISA and proteasome activity was determined by fluorometric peptidaseassay. Treatment with GS Rg1 40 mg/kg resulted in a significantly lower infarct volume and improved the neurological deficit score as well as the histological appearance compared to the control I/R group (P < 0.05). GS Rg1 treatment resulted in significantly lower proinflammatory cytokine expressions and suppression of the nuclear translocation of NF-κB as well as the phosphorylation of IκBα (P < 0.01). Finally, GS Rg1 treatment decreased the proteasomal activity and protein aggregate accumulation in brain tissues (P < 0.01). Our results confirm the neuroprotective function of GS Rg1 at 40 mg/kg. This effect may be attributed to a decrease in ubiquitinated aggregates and a suppression of the inflammatory response after I/R insult. Ginsenoside Rg1 Stroke Ubiquitinated aggregates Inflammatory response Proteasome Jiang, Hong verfasserin aut Jin, Rihua verfasserin aut Zhao, Yiming verfasserin aut Bai, Yang verfasserin aut Xu, Haiyang verfasserin aut Chen, Yong verfasserin aut Enthalten in European journal of pharmacology New York, NY [u.a.] : Elsevier, 1967 853, Seite 65-73 Online-Ressource (DE-627)300897340 (DE-600)1483526-5 (DE-576)081952627 1879-0712 nnns volume:853 pages:65-73 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 853 65-73
language	English
source	Enthalten in European journal of pharmacology 853, Seite 65-73 volume:853 pages:65-73
sourceStr	Enthalten in European journal of pharmacology 853, Seite 65-73 volume:853 pages:65-73
format_phy_str_mv	Article
bklname	Pharmakologie
institution	findex.gbv.de
topic_facet	Ginsenoside Rg1 Stroke Ubiquitinated aggregates Inflammatory response Proteasome
dewey-raw	610
isfreeaccess_bool	false
container_title	European journal of pharmacology
authorswithroles_txt_mv	Zheng, Tianyang @@aut@@ Jiang, Hong @@aut@@ Jin, Rihua @@aut@@ Zhao, Yiming @@aut@@ Bai, Yang @@aut@@ Xu, Haiyang @@aut@@ Chen, Yong @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
hierarchy_top_id	300897340
dewey-sort	3610
id	ELV00217507X
language_de	englisch
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Treatment with GS Rg1 40 mg/kg resulted in a significantly lower infarct volume and improved the neurological deficit score as well as the histological appearance compared to the control I/R group (P < 0.05). GS Rg1 treatment resulted in significantly lower proinflammatory cytokine expressions and suppression of the nuclear translocation of NF-κB as well as the phosphorylation of IκBα (P < 0.01). Finally, GS Rg1 treatment decreased the proteasomal activity and protein aggregate accumulation in brain tissues (P < 0.01). Our results confirm the neuroprotective function of GS Rg1 at 40 mg/kg. 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author	Zheng, Tianyang
spellingShingle	Zheng, Tianyang ddc 610 fid PHARM bkl 44.38 misc Ginsenoside Rg1 misc Stroke misc Ubiquitinated aggregates misc Inflammatory response misc Proteasome Ginsenoside Rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury
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topic_title	610 DE-600 PHARM DE-84 fid 44.38 bkl Ginsenoside Rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury Ginsenoside Rg1 Stroke Ubiquitinated aggregates Inflammatory response Proteasome
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title	Ginsenoside Rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury
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title_full	Ginsenoside Rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury
author_sort	Zheng, Tianyang
journal	European journal of pharmacology
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title_sort	ginsenoside rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury
title_auth	Ginsenoside Rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury
abstract	Ginsenoside Rg1 (GS Rg1) is a glycosylated triterpenoid saponin extracted from Panax ginseng. We aim to investigate the impact of GS Rg1 on protein aggregation and inflammatory response in a cerebral ischemia/reperfusion (I/R) injury model. Rats were administered different doses of GS Rg1 (10, 20, or 40 mg/kg/day) or nimodipine (1 mg/kg/day) for 5 consecutive days. Cerebral I/R injury was induced by middle cerebral artery occlusion for 2 h followed by a 22 h reperfusion period. Next, we examined the differences in infarct volume and neurological deficit via TTC staining and Longa′s scoring, respectively. Furthermore, the differences in protein aggregates, proteasome, IκBα and NF-κB in the cerebral cortices were investigated through western blotting. The distribution of ubiquitin, proteasome and NF-κB in the neocortex were examined through immunohistochemistry. Pro-inflammatory cytokines were measured using ELISA and proteasome activity was determined by fluorometric peptidaseassay. Treatment with GS Rg1 40 mg/kg resulted in a significantly lower infarct volume and improved the neurological deficit score as well as the histological appearance compared to the control I/R group (P < 0.05). GS Rg1 treatment resulted in significantly lower proinflammatory cytokine expressions and suppression of the nuclear translocation of NF-κB as well as the phosphorylation of IκBα (P < 0.01). Finally, GS Rg1 treatment decreased the proteasomal activity and protein aggregate accumulation in brain tissues (P < 0.01). Our results confirm the neuroprotective function of GS Rg1 at 40 mg/kg. This effect may be attributed to a decrease in ubiquitinated aggregates and a suppression of the inflammatory response after I/R insult.
abstractGer	Ginsenoside Rg1 (GS Rg1) is a glycosylated triterpenoid saponin extracted from Panax ginseng. We aim to investigate the impact of GS Rg1 on protein aggregation and inflammatory response in a cerebral ischemia/reperfusion (I/R) injury model. Rats were administered different doses of GS Rg1 (10, 20, or 40 mg/kg/day) or nimodipine (1 mg/kg/day) for 5 consecutive days. Cerebral I/R injury was induced by middle cerebral artery occlusion for 2 h followed by a 22 h reperfusion period. Next, we examined the differences in infarct volume and neurological deficit via TTC staining and Longa′s scoring, respectively. Furthermore, the differences in protein aggregates, proteasome, IκBα and NF-κB in the cerebral cortices were investigated through western blotting. The distribution of ubiquitin, proteasome and NF-κB in the neocortex were examined through immunohistochemistry. Pro-inflammatory cytokines were measured using ELISA and proteasome activity was determined by fluorometric peptidaseassay. Treatment with GS Rg1 40 mg/kg resulted in a significantly lower infarct volume and improved the neurological deficit score as well as the histological appearance compared to the control I/R group (P < 0.05). GS Rg1 treatment resulted in significantly lower proinflammatory cytokine expressions and suppression of the nuclear translocation of NF-κB as well as the phosphorylation of IκBα (P < 0.01). Finally, GS Rg1 treatment decreased the proteasomal activity and protein aggregate accumulation in brain tissues (P < 0.01). Our results confirm the neuroprotective function of GS Rg1 at 40 mg/kg. This effect may be attributed to a decrease in ubiquitinated aggregates and a suppression of the inflammatory response after I/R insult.
abstract_unstemmed	Ginsenoside Rg1 (GS Rg1) is a glycosylated triterpenoid saponin extracted from Panax ginseng. We aim to investigate the impact of GS Rg1 on protein aggregation and inflammatory response in a cerebral ischemia/reperfusion (I/R) injury model. Rats were administered different doses of GS Rg1 (10, 20, or 40 mg/kg/day) or nimodipine (1 mg/kg/day) for 5 consecutive days. Cerebral I/R injury was induced by middle cerebral artery occlusion for 2 h followed by a 22 h reperfusion period. Next, we examined the differences in infarct volume and neurological deficit via TTC staining and Longa′s scoring, respectively. Furthermore, the differences in protein aggregates, proteasome, IκBα and NF-κB in the cerebral cortices were investigated through western blotting. The distribution of ubiquitin, proteasome and NF-κB in the neocortex were examined through immunohistochemistry. Pro-inflammatory cytokines were measured using ELISA and proteasome activity was determined by fluorometric peptidaseassay. Treatment with GS Rg1 40 mg/kg resulted in a significantly lower infarct volume and improved the neurological deficit score as well as the histological appearance compared to the control I/R group (P < 0.05). GS Rg1 treatment resulted in significantly lower proinflammatory cytokine expressions and suppression of the nuclear translocation of NF-κB as well as the phosphorylation of IκBα (P < 0.01). Finally, GS Rg1 treatment decreased the proteasomal activity and protein aggregate accumulation in brain tissues (P < 0.01). Our results confirm the neuroprotective function of GS Rg1 at 40 mg/kg. This effect may be attributed to a decrease in ubiquitinated aggregates and a suppression of the inflammatory response after I/R insult.
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title_short	Ginsenoside Rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury
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author2	Jiang, Hong Jin, Rihua Zhao, Yiming Bai, Yang Xu, Haiyang Chen, Yong
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up_date	2024-07-06T23:51:50.330Z
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Ginsenoside Rg1 attenuates protein aggregation and inflammatory response following cerebral ischemia and reperfusion injury

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