Hypolipidemic effect of ethanol extract from Chimonanthus nitens Oliv. leaves in hyperlipidemia rats via activation of the leptin/JAK2/STAT3 pathway

Background This study aims to explore the protective role of ethanol extract from Chimonanthus nitens Oliv. leaf (COE) in hyperlipidemia via the leptin/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. Methods Male Sprague‒Dawley rats were randomly divided int...
Ausführliche Beschreibung

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Autor*in:	Pan, Jianping [verfasserIn] Ouyang, Xilin Jin, Qi Wang, Wei Xie, Jiali Yu, Baoming Ling, Zhijie Wu, Qizhen Zheng, Baoping

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	Oliv. leaf Hyperlipidemia Leptin/JAK2/STAT3 pathway Lipid metabolism Oxidative stress

Anmerkung:	© The Author(s) 2022

Übergeordnetes Werk:	Enthalten in: Molecular medicine - [London] : BioMed Central, 1994, 28(2022), 1 vom: Dez.
Übergeordnetes Werk:	volume:28 ; year:2022 ; number:1 ; month:12

Links:	Volltext

DOI / URN:	10.1186/s10020-022-00589-z

Katalog-ID:	SPR051248824

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245	1	0	\|a Hypolipidemic effect of ethanol extract from Chimonanthus nitens Oliv. leaves in hyperlipidemia rats via activation of the leptin/JAK2/STAT3 pathway
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520			\|a Background This study aims to explore the protective role of ethanol extract from Chimonanthus nitens Oliv. leaf (COE) in hyperlipidemia via the leptin/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. Methods Male Sprague‒Dawley rats were randomly divided into 6 groups (n = 8): normal-fat diet (NMD), high-fat diet (HFD), HFD treated with simvastatin (SIM, 5 mg/kg/day), and HFD treated with COE (40, 80, 160 mg/kg/day). Lipid parameters, oxidative stress factors, serum leptin, body weight, hepatic wet weight and liver index were measured. Proteins in the leptin/JAK2/STAT3 pathway in liver tissues were determined using western blotting. Additionally, the expression levels of cytochrome P450 family 7 subfamily A member 1 (CYP7A1) and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) were quantified using western blotting and quantitative real-time polymerase chain reaction (qPCR). Results COE decreased HFD-induced increases in body weight, hepatic wet weight and the liver index. HFD-induced hyperlipidemia and oxidative stress were observed in rat serum and livers. Additionally, COE repressed these two symptoms in rats fed a HFD. Moreover, COE caused CYP7A1 upregulation and HMGCR downregulation in HFD-fed rats. Mechanistically, COE induced the expression of leptin receptor (OB-Rb) and JAK2 and STAT3 phosphorylation in HFD-treated rats. Conclusion COE activates the leptin/JAK2/STAT3 pathway, leading to an improvement in liver function and lipid metabolism and ultimately alleviating hyperlipidemia in rats. Therefore, COE may be a potential hypolipidemic drug for the treatment of hyperlipidemia.
520			\|a Highlights COE improves lipid levels and lipase activities in hyperlipidemic rats.COE ameliorates antioxidant enzyme activities and liver function in hyperlipidemic rats.COE exerts a hypolipidemic effect by activating the leptin/JAK2/STAT3 pathway.
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allfields	10.1186/s10020-022-00589-z doi (DE-627)SPR051248824 (SPR)s10020-022-00589-z-e DE-627 ger DE-627 rakwb eng Pan, Jianping verfasserin aut Hypolipidemic effect of ethanol extract from Chimonanthus nitens Oliv. leaves in hyperlipidemia rats via activation of the leptin/JAK2/STAT3 pathway 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background This study aims to explore the protective role of ethanol extract from Chimonanthus nitens Oliv. leaf (COE) in hyperlipidemia via the leptin/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. Methods Male Sprague‒Dawley rats were randomly divided into 6 groups (n = 8): normal-fat diet (NMD), high-fat diet (HFD), HFD treated with simvastatin (SIM, 5 mg/kg/day), and HFD treated with COE (40, 80, 160 mg/kg/day). Lipid parameters, oxidative stress factors, serum leptin, body weight, hepatic wet weight and liver index were measured. Proteins in the leptin/JAK2/STAT3 pathway in liver tissues were determined using western blotting. Additionally, the expression levels of cytochrome P450 family 7 subfamily A member 1 (CYP7A1) and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) were quantified using western blotting and quantitative real-time polymerase chain reaction (qPCR). Results COE decreased HFD-induced increases in body weight, hepatic wet weight and the liver index. HFD-induced hyperlipidemia and oxidative stress were observed in rat serum and livers. Additionally, COE repressed these two symptoms in rats fed a HFD. Moreover, COE caused CYP7A1 upregulation and HMGCR downregulation in HFD-fed rats. Mechanistically, COE induced the expression of leptin receptor (OB-Rb) and JAK2 and STAT3 phosphorylation in HFD-treated rats. Conclusion COE activates the leptin/JAK2/STAT3 pathway, leading to an improvement in liver function and lipid metabolism and ultimately alleviating hyperlipidemia in rats. Therefore, COE may be a potential hypolipidemic drug for the treatment of hyperlipidemia. Highlights COE improves lipid levels and lipase activities in hyperlipidemic rats.COE ameliorates antioxidant enzyme activities and liver function in hyperlipidemic rats.COE exerts a hypolipidemic effect by activating the leptin/JAK2/STAT3 pathway. Oliv. leaf (dpeaa)DE-He213 Hyperlipidemia (dpeaa)DE-He213 Leptin/JAK2/STAT3 pathway (dpeaa)DE-He213 Lipid metabolism (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Ouyang, Xilin aut Jin, Qi aut Wang, Wei aut Xie, Jiali aut Yu, Baoming aut Ling, Zhijie aut Wu, Qizhen aut Zheng, Baoping (orcid)0000-0001-9434-3810 aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 28(2022), 1 vom: Dez. (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:28 year:2022 number:1 month:12 https://dx.doi.org/10.1186/s10020-022-00589-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 28 2022 1 12
spelling	10.1186/s10020-022-00589-z doi (DE-627)SPR051248824 (SPR)s10020-022-00589-z-e DE-627 ger DE-627 rakwb eng Pan, Jianping verfasserin aut Hypolipidemic effect of ethanol extract from Chimonanthus nitens Oliv. leaves in hyperlipidemia rats via activation of the leptin/JAK2/STAT3 pathway 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background This study aims to explore the protective role of ethanol extract from Chimonanthus nitens Oliv. leaf (COE) in hyperlipidemia via the leptin/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. Methods Male Sprague‒Dawley rats were randomly divided into 6 groups (n = 8): normal-fat diet (NMD), high-fat diet (HFD), HFD treated with simvastatin (SIM, 5 mg/kg/day), and HFD treated with COE (40, 80, 160 mg/kg/day). Lipid parameters, oxidative stress factors, serum leptin, body weight, hepatic wet weight and liver index were measured. Proteins in the leptin/JAK2/STAT3 pathway in liver tissues were determined using western blotting. Additionally, the expression levels of cytochrome P450 family 7 subfamily A member 1 (CYP7A1) and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) were quantified using western blotting and quantitative real-time polymerase chain reaction (qPCR). Results COE decreased HFD-induced increases in body weight, hepatic wet weight and the liver index. HFD-induced hyperlipidemia and oxidative stress were observed in rat serum and livers. Additionally, COE repressed these two symptoms in rats fed a HFD. Moreover, COE caused CYP7A1 upregulation and HMGCR downregulation in HFD-fed rats. Mechanistically, COE induced the expression of leptin receptor (OB-Rb) and JAK2 and STAT3 phosphorylation in HFD-treated rats. Conclusion COE activates the leptin/JAK2/STAT3 pathway, leading to an improvement in liver function and lipid metabolism and ultimately alleviating hyperlipidemia in rats. Therefore, COE may be a potential hypolipidemic drug for the treatment of hyperlipidemia. Highlights COE improves lipid levels and lipase activities in hyperlipidemic rats.COE ameliorates antioxidant enzyme activities and liver function in hyperlipidemic rats.COE exerts a hypolipidemic effect by activating the leptin/JAK2/STAT3 pathway. Oliv. leaf (dpeaa)DE-He213 Hyperlipidemia (dpeaa)DE-He213 Leptin/JAK2/STAT3 pathway (dpeaa)DE-He213 Lipid metabolism (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Ouyang, Xilin aut Jin, Qi aut Wang, Wei aut Xie, Jiali aut Yu, Baoming aut Ling, Zhijie aut Wu, Qizhen aut Zheng, Baoping (orcid)0000-0001-9434-3810 aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 28(2022), 1 vom: Dez. (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:28 year:2022 number:1 month:12 https://dx.doi.org/10.1186/s10020-022-00589-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 28 2022 1 12
allfields_unstemmed	10.1186/s10020-022-00589-z doi (DE-627)SPR051248824 (SPR)s10020-022-00589-z-e DE-627 ger DE-627 rakwb eng Pan, Jianping verfasserin aut Hypolipidemic effect of ethanol extract from Chimonanthus nitens Oliv. leaves in hyperlipidemia rats via activation of the leptin/JAK2/STAT3 pathway 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background This study aims to explore the protective role of ethanol extract from Chimonanthus nitens Oliv. leaf (COE) in hyperlipidemia via the leptin/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. Methods Male Sprague‒Dawley rats were randomly divided into 6 groups (n = 8): normal-fat diet (NMD), high-fat diet (HFD), HFD treated with simvastatin (SIM, 5 mg/kg/day), and HFD treated with COE (40, 80, 160 mg/kg/day). Lipid parameters, oxidative stress factors, serum leptin, body weight, hepatic wet weight and liver index were measured. Proteins in the leptin/JAK2/STAT3 pathway in liver tissues were determined using western blotting. Additionally, the expression levels of cytochrome P450 family 7 subfamily A member 1 (CYP7A1) and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) were quantified using western blotting and quantitative real-time polymerase chain reaction (qPCR). Results COE decreased HFD-induced increases in body weight, hepatic wet weight and the liver index. HFD-induced hyperlipidemia and oxidative stress were observed in rat serum and livers. Additionally, COE repressed these two symptoms in rats fed a HFD. Moreover, COE caused CYP7A1 upregulation and HMGCR downregulation in HFD-fed rats. Mechanistically, COE induced the expression of leptin receptor (OB-Rb) and JAK2 and STAT3 phosphorylation in HFD-treated rats. Conclusion COE activates the leptin/JAK2/STAT3 pathway, leading to an improvement in liver function and lipid metabolism and ultimately alleviating hyperlipidemia in rats. Therefore, COE may be a potential hypolipidemic drug for the treatment of hyperlipidemia. Highlights COE improves lipid levels and lipase activities in hyperlipidemic rats.COE ameliorates antioxidant enzyme activities and liver function in hyperlipidemic rats.COE exerts a hypolipidemic effect by activating the leptin/JAK2/STAT3 pathway. Oliv. leaf (dpeaa)DE-He213 Hyperlipidemia (dpeaa)DE-He213 Leptin/JAK2/STAT3 pathway (dpeaa)DE-He213 Lipid metabolism (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Ouyang, Xilin aut Jin, Qi aut Wang, Wei aut Xie, Jiali aut Yu, Baoming aut Ling, Zhijie aut Wu, Qizhen aut Zheng, Baoping (orcid)0000-0001-9434-3810 aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 28(2022), 1 vom: Dez. (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:28 year:2022 number:1 month:12 https://dx.doi.org/10.1186/s10020-022-00589-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 28 2022 1 12
allfieldsGer	10.1186/s10020-022-00589-z doi (DE-627)SPR051248824 (SPR)s10020-022-00589-z-e DE-627 ger DE-627 rakwb eng Pan, Jianping verfasserin aut Hypolipidemic effect of ethanol extract from Chimonanthus nitens Oliv. leaves in hyperlipidemia rats via activation of the leptin/JAK2/STAT3 pathway 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background This study aims to explore the protective role of ethanol extract from Chimonanthus nitens Oliv. leaf (COE) in hyperlipidemia via the leptin/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. Methods Male Sprague‒Dawley rats were randomly divided into 6 groups (n = 8): normal-fat diet (NMD), high-fat diet (HFD), HFD treated with simvastatin (SIM, 5 mg/kg/day), and HFD treated with COE (40, 80, 160 mg/kg/day). Lipid parameters, oxidative stress factors, serum leptin, body weight, hepatic wet weight and liver index were measured. Proteins in the leptin/JAK2/STAT3 pathway in liver tissues were determined using western blotting. Additionally, the expression levels of cytochrome P450 family 7 subfamily A member 1 (CYP7A1) and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) were quantified using western blotting and quantitative real-time polymerase chain reaction (qPCR). Results COE decreased HFD-induced increases in body weight, hepatic wet weight and the liver index. HFD-induced hyperlipidemia and oxidative stress were observed in rat serum and livers. Additionally, COE repressed these two symptoms in rats fed a HFD. Moreover, COE caused CYP7A1 upregulation and HMGCR downregulation in HFD-fed rats. Mechanistically, COE induced the expression of leptin receptor (OB-Rb) and JAK2 and STAT3 phosphorylation in HFD-treated rats. Conclusion COE activates the leptin/JAK2/STAT3 pathway, leading to an improvement in liver function and lipid metabolism and ultimately alleviating hyperlipidemia in rats. Therefore, COE may be a potential hypolipidemic drug for the treatment of hyperlipidemia. Highlights COE improves lipid levels and lipase activities in hyperlipidemic rats.COE ameliorates antioxidant enzyme activities and liver function in hyperlipidemic rats.COE exerts a hypolipidemic effect by activating the leptin/JAK2/STAT3 pathway. Oliv. leaf (dpeaa)DE-He213 Hyperlipidemia (dpeaa)DE-He213 Leptin/JAK2/STAT3 pathway (dpeaa)DE-He213 Lipid metabolism (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Ouyang, Xilin aut Jin, Qi aut Wang, Wei aut Xie, Jiali aut Yu, Baoming aut Ling, Zhijie aut Wu, Qizhen aut Zheng, Baoping (orcid)0000-0001-9434-3810 aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 28(2022), 1 vom: Dez. (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:28 year:2022 number:1 month:12 https://dx.doi.org/10.1186/s10020-022-00589-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 28 2022 1 12
allfieldsSound	10.1186/s10020-022-00589-z doi (DE-627)SPR051248824 (SPR)s10020-022-00589-z-e DE-627 ger DE-627 rakwb eng Pan, Jianping verfasserin aut Hypolipidemic effect of ethanol extract from Chimonanthus nitens Oliv. leaves in hyperlipidemia rats via activation of the leptin/JAK2/STAT3 pathway 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background This study aims to explore the protective role of ethanol extract from Chimonanthus nitens Oliv. leaf (COE) in hyperlipidemia via the leptin/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. Methods Male Sprague‒Dawley rats were randomly divided into 6 groups (n = 8): normal-fat diet (NMD), high-fat diet (HFD), HFD treated with simvastatin (SIM, 5 mg/kg/day), and HFD treated with COE (40, 80, 160 mg/kg/day). Lipid parameters, oxidative stress factors, serum leptin, body weight, hepatic wet weight and liver index were measured. Proteins in the leptin/JAK2/STAT3 pathway in liver tissues were determined using western blotting. Additionally, the expression levels of cytochrome P450 family 7 subfamily A member 1 (CYP7A1) and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) were quantified using western blotting and quantitative real-time polymerase chain reaction (qPCR). Results COE decreased HFD-induced increases in body weight, hepatic wet weight and the liver index. HFD-induced hyperlipidemia and oxidative stress were observed in rat serum and livers. Additionally, COE repressed these two symptoms in rats fed a HFD. Moreover, COE caused CYP7A1 upregulation and HMGCR downregulation in HFD-fed rats. Mechanistically, COE induced the expression of leptin receptor (OB-Rb) and JAK2 and STAT3 phosphorylation in HFD-treated rats. Conclusion COE activates the leptin/JAK2/STAT3 pathway, leading to an improvement in liver function and lipid metabolism and ultimately alleviating hyperlipidemia in rats. Therefore, COE may be a potential hypolipidemic drug for the treatment of hyperlipidemia. Highlights COE improves lipid levels and lipase activities in hyperlipidemic rats.COE ameliorates antioxidant enzyme activities and liver function in hyperlipidemic rats.COE exerts a hypolipidemic effect by activating the leptin/JAK2/STAT3 pathway. Oliv. leaf (dpeaa)DE-He213 Hyperlipidemia (dpeaa)DE-He213 Leptin/JAK2/STAT3 pathway (dpeaa)DE-He213 Lipid metabolism (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Ouyang, Xilin aut Jin, Qi aut Wang, Wei aut Xie, Jiali aut Yu, Baoming aut Ling, Zhijie aut Wu, Qizhen aut Zheng, Baoping (orcid)0000-0001-9434-3810 aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 28(2022), 1 vom: Dez. (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:28 year:2022 number:1 month:12 https://dx.doi.org/10.1186/s10020-022-00589-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 28 2022 1 12
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authorswithroles_txt_mv	Pan, Jianping @@aut@@ Ouyang, Xilin @@aut@@ Jin, Qi @@aut@@ Wang, Wei @@aut@@ Xie, Jiali @@aut@@ Yu, Baoming @@aut@@ Ling, Zhijie @@aut@@ Wu, Qizhen @@aut@@ Zheng, Baoping @@aut@@
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author	Pan, Jianping
spellingShingle	Pan, Jianping misc Oliv. leaf misc Hyperlipidemia misc Leptin/JAK2/STAT3 pathway misc Lipid metabolism misc Oxidative stress Hypolipidemic effect of ethanol extract from Chimonanthus nitens Oliv. leaves in hyperlipidemia rats via activation of the leptin/JAK2/STAT3 pathway
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topic_title	Hypolipidemic effect of ethanol extract from Chimonanthus nitens Oliv. leaves in hyperlipidemia rats via activation of the leptin/JAK2/STAT3 pathway Oliv. leaf (dpeaa)DE-He213 Hyperlipidemia (dpeaa)DE-He213 Leptin/JAK2/STAT3 pathway (dpeaa)DE-He213 Lipid metabolism (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213
topic	misc Oliv. leaf misc Hyperlipidemia misc Leptin/JAK2/STAT3 pathway misc Lipid metabolism misc Oxidative stress
topic_unstemmed	misc Oliv. leaf misc Hyperlipidemia misc Leptin/JAK2/STAT3 pathway misc Lipid metabolism misc Oxidative stress
topic_browse	misc Oliv. leaf misc Hyperlipidemia misc Leptin/JAK2/STAT3 pathway misc Lipid metabolism misc Oxidative stress
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title	Hypolipidemic effect of ethanol extract from Chimonanthus nitens Oliv. leaves in hyperlipidemia rats via activation of the leptin/JAK2/STAT3 pathway
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title_full	Hypolipidemic effect of ethanol extract from Chimonanthus nitens Oliv. leaves in hyperlipidemia rats via activation of the leptin/JAK2/STAT3 pathway
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title_sort	hypolipidemic effect of ethanol extract from chimonanthus nitens oliv. leaves in hyperlipidemia rats via activation of the leptin/jak2/stat3 pathway
title_auth	Hypolipidemic effect of ethanol extract from Chimonanthus nitens Oliv. leaves in hyperlipidemia rats via activation of the leptin/JAK2/STAT3 pathway
abstract	Background This study aims to explore the protective role of ethanol extract from Chimonanthus nitens Oliv. leaf (COE) in hyperlipidemia via the leptin/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. Methods Male Sprague‒Dawley rats were randomly divided into 6 groups (n = 8): normal-fat diet (NMD), high-fat diet (HFD), HFD treated with simvastatin (SIM, 5 mg/kg/day), and HFD treated with COE (40, 80, 160 mg/kg/day). Lipid parameters, oxidative stress factors, serum leptin, body weight, hepatic wet weight and liver index were measured. Proteins in the leptin/JAK2/STAT3 pathway in liver tissues were determined using western blotting. Additionally, the expression levels of cytochrome P450 family 7 subfamily A member 1 (CYP7A1) and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) were quantified using western blotting and quantitative real-time polymerase chain reaction (qPCR). Results COE decreased HFD-induced increases in body weight, hepatic wet weight and the liver index. HFD-induced hyperlipidemia and oxidative stress were observed in rat serum and livers. Additionally, COE repressed these two symptoms in rats fed a HFD. Moreover, COE caused CYP7A1 upregulation and HMGCR downregulation in HFD-fed rats. Mechanistically, COE induced the expression of leptin receptor (OB-Rb) and JAK2 and STAT3 phosphorylation in HFD-treated rats. Conclusion COE activates the leptin/JAK2/STAT3 pathway, leading to an improvement in liver function and lipid metabolism and ultimately alleviating hyperlipidemia in rats. Therefore, COE may be a potential hypolipidemic drug for the treatment of hyperlipidemia. Highlights COE improves lipid levels and lipase activities in hyperlipidemic rats.COE ameliorates antioxidant enzyme activities and liver function in hyperlipidemic rats.COE exerts a hypolipidemic effect by activating the leptin/JAK2/STAT3 pathway. © The Author(s) 2022
abstractGer	Background This study aims to explore the protective role of ethanol extract from Chimonanthus nitens Oliv. leaf (COE) in hyperlipidemia via the leptin/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. Methods Male Sprague‒Dawley rats were randomly divided into 6 groups (n = 8): normal-fat diet (NMD), high-fat diet (HFD), HFD treated with simvastatin (SIM, 5 mg/kg/day), and HFD treated with COE (40, 80, 160 mg/kg/day). Lipid parameters, oxidative stress factors, serum leptin, body weight, hepatic wet weight and liver index were measured. Proteins in the leptin/JAK2/STAT3 pathway in liver tissues were determined using western blotting. Additionally, the expression levels of cytochrome P450 family 7 subfamily A member 1 (CYP7A1) and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) were quantified using western blotting and quantitative real-time polymerase chain reaction (qPCR). Results COE decreased HFD-induced increases in body weight, hepatic wet weight and the liver index. HFD-induced hyperlipidemia and oxidative stress were observed in rat serum and livers. Additionally, COE repressed these two symptoms in rats fed a HFD. Moreover, COE caused CYP7A1 upregulation and HMGCR downregulation in HFD-fed rats. Mechanistically, COE induced the expression of leptin receptor (OB-Rb) and JAK2 and STAT3 phosphorylation in HFD-treated rats. Conclusion COE activates the leptin/JAK2/STAT3 pathway, leading to an improvement in liver function and lipid metabolism and ultimately alleviating hyperlipidemia in rats. Therefore, COE may be a potential hypolipidemic drug for the treatment of hyperlipidemia. Highlights COE improves lipid levels and lipase activities in hyperlipidemic rats.COE ameliorates antioxidant enzyme activities and liver function in hyperlipidemic rats.COE exerts a hypolipidemic effect by activating the leptin/JAK2/STAT3 pathway. © The Author(s) 2022
abstract_unstemmed	Background This study aims to explore the protective role of ethanol extract from Chimonanthus nitens Oliv. leaf (COE) in hyperlipidemia via the leptin/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. Methods Male Sprague‒Dawley rats were randomly divided into 6 groups (n = 8): normal-fat diet (NMD), high-fat diet (HFD), HFD treated with simvastatin (SIM, 5 mg/kg/day), and HFD treated with COE (40, 80, 160 mg/kg/day). Lipid parameters, oxidative stress factors, serum leptin, body weight, hepatic wet weight and liver index were measured. Proteins in the leptin/JAK2/STAT3 pathway in liver tissues were determined using western blotting. Additionally, the expression levels of cytochrome P450 family 7 subfamily A member 1 (CYP7A1) and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) were quantified using western blotting and quantitative real-time polymerase chain reaction (qPCR). Results COE decreased HFD-induced increases in body weight, hepatic wet weight and the liver index. HFD-induced hyperlipidemia and oxidative stress were observed in rat serum and livers. Additionally, COE repressed these two symptoms in rats fed a HFD. Moreover, COE caused CYP7A1 upregulation and HMGCR downregulation in HFD-fed rats. Mechanistically, COE induced the expression of leptin receptor (OB-Rb) and JAK2 and STAT3 phosphorylation in HFD-treated rats. Conclusion COE activates the leptin/JAK2/STAT3 pathway, leading to an improvement in liver function and lipid metabolism and ultimately alleviating hyperlipidemia in rats. Therefore, COE may be a potential hypolipidemic drug for the treatment of hyperlipidemia. Highlights COE improves lipid levels and lipase activities in hyperlipidemic rats.COE ameliorates antioxidant enzyme activities and liver function in hyperlipidemic rats.COE exerts a hypolipidemic effect by activating the leptin/JAK2/STAT3 pathway. © The Author(s) 2022
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container_issue	1
title_short	Hypolipidemic effect of ethanol extract from Chimonanthus nitens Oliv. leaves in hyperlipidemia rats via activation of the leptin/JAK2/STAT3 pathway
url	https://dx.doi.org/10.1186/s10020-022-00589-z
remote_bool	true
author2	Ouyang, Xilin Jin, Qi Wang, Wei Xie, Jiali Yu, Baoming Ling, Zhijie Wu, Qizhen Zheng, Baoping
author2Str	Ouyang, Xilin Jin, Qi Wang, Wei Xie, Jiali Yu, Baoming Ling, Zhijie Wu, Qizhen Zheng, Baoping
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doi_str	10.1186/s10020-022-00589-z
up_date	2024-07-03T20:41:35.150Z
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Hypolipidemic effect of ethanol extract from Chimonanthus nitens Oliv. leaves in hyperlipidemia rats via activation of the leptin/JAK2/STAT3 pathway

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