BabaoDan attenuates high-fat diet-induced non-alcoholic fatty liver disease via activation of AMPK signaling
Babaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease progression, but little is known about its effect on non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the effects of BBD on ob...
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Published in | Cell & bioscience Vol. 9; no. 1; pp. 77 - 10 |
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Main Authors | , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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BioMed Central Ltd
18.09.2019
BioMed Central BMC |
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Abstract | Babaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease progression, but little is known about its effect on non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the effects of BBD on obesity-induced NAFLD.
C57BL/6 J mice were fed with normal diet, high fat diet (HFD) or HFD + BBD for 8 weeks. Weights of all mice were recorded every 3 days. At the end of the experiments, the level of livers, kidneys and adipose tissues of each animal was weighed. Blood serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) cholesterol, low density lipoprotein cholesterol (LDL-C), glucose and leptin were detected with appropriate test kits. Haematoxylin-eosin (HE), Masson trichrome and Oil Red O staining of the liver were performed. We applied immunohistochemical analysis to investigate the expression of TNF-α, IL-6 and leptin in liver tissue. The expression of genes related lipid anabolism (SREBP1-c, ACC, SCD-1, LXRα and CD36) and ß-oxidation (CPT-1 and PPARα) in liver and adipose tissues was determined by RT-PCR. The expression of AMPK and p-AMPK was determined by western blot analysis.
We found the weight of bodies and tissues (retroperitoneal fat pads, kidneys and livers) of mice fed with HFD + BBD were significantly lower than that of HFD-fed mice. And liver injury induced by HFD was relieved in mice treated with BBD, accompanied with significant reduction were observed in serum ALT/AST activities and alleviated pathological damage. The levels of glucose, TG, TC, HDL-C and LDL-C in the liver or serum were significantly decreased on HFD + BBD group compared with HFD group. Furthermore, BBD treatment reduced the level of TNF-α and IL-6 induced by HFD. The level of leptin in the liver and serum were reduced in mice fed with HFD + BBD than that of HFD-fed mice. Several lipid synthesis genes (SREBP1-c, ACC, SCD-1, LXRα and CD36) were down-regulated and that of ß-oxidation (CPT-1 and PPARα) up-regulated in HFD + BBD group compared with HFD group. In addition, BBD increased the expression of p-AMPK compared with untreated HFD group, which suggested BBD improved the activation of AMPK pathway.
In summary, our results indicate that BBD has potential applications in the prevention and treatment of NAFLD, which may be closely related to its effect on lipid metabolism via activation of AMPK signaling. |
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AbstractList | Background Babaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease progression, but little is known about its effect on non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the effects of BBD on obesity-induced NAFLD. Methods C57BL/6 J mice were fed with normal diet, high fat diet (HFD) or HFD + BBD for 8 weeks. Weights of all mice were recorded every 3 days. At the end of the experiments, the level of livers, kidneys and adipose tissues of each animal was weighed. Blood serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) cholesterol, low density lipoprotein cholesterol (LDL-C), glucose and leptin were detected with appropriate test kits. Haematoxylin-eosin (HE), Masson trichrome and Oil Red O staining of the liver were performed. We applied immunohistochemical analysis to investigate the expression of TNF-[alpha], IL-6 and leptin in liver tissue. The expression of genes related lipid anabolism (SREBP1-c, ACC, SCD-1, LXR[alpha] and CD36) and ss-oxidation (CPT-1 and PPAR[alpha]) in liver and adipose tissues was determined by RT-PCR. The expression of AMPK and p-AMPK was determined by western blot analysis. Results We found the weight of bodies and tissues (retroperitoneal fat pads, kidneys and livers) of mice fed with HFD + BBD were significantly lower than that of HFD-fed mice. And liver injury induced by HFD was relieved in mice treated with BBD, accompanied with significant reduction were observed in serum ALT/AST activities and alleviated pathological damage. The levels of glucose, TG, TC, HDL-C and LDL-C in the liver or serum were significantly decreased on HFD + BBD group compared with HFD group. Furthermore, BBD treatment reduced the level of TNF-[alpha] and IL-6 induced by HFD. The level of leptin in the liver and serum were reduced in mice fed with HFD + BBD than that of HFD-fed mice. Several lipid synthesis genes (SREBP1-c, ACC, SCD-1, LXR[alpha] and CD36) were down-regulated and that of ss-oxidation (CPT-1 and PPAR[alpha]) up-regulated in HFD + BBD group compared with HFD group. In addition, BBD increased the expression of p-AMPK compared with untreated HFD group, which suggested BBD improved the activation of AMPK pathway. Conclusion In summary, our results indicate that BBD has potential applications in the prevention and treatment of NAFLD, which may be closely related to its effect on lipid metabolism via activation of AMPK signaling. Keywords: Babaodan, Non-alcoholic fatty liver disease, Lipid metabolism, AMPK pathway Babaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease progression, but little is known about its effect on non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the effects of BBD on obesity-induced NAFLD. C57BL/6 J mice were fed with normal diet, high fat diet (HFD) or HFD + BBD for 8 weeks. Weights of all mice were recorded every 3 days. At the end of the experiments, the level of livers, kidneys and adipose tissues of each animal was weighed. Blood serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) cholesterol, low density lipoprotein cholesterol (LDL-C), glucose and leptin were detected with appropriate test kits. Haematoxylin-eosin (HE), Masson trichrome and Oil Red O staining of the liver were performed. We applied immunohistochemical analysis to investigate the expression of TNF-[alpha], IL-6 and leptin in liver tissue. The expression of genes related lipid anabolism (SREBP1-c, ACC, SCD-1, LXR[alpha] and CD36) and ss-oxidation (CPT-1 and PPAR[alpha]) in liver and adipose tissues was determined by RT-PCR. The expression of AMPK and p-AMPK was determined by western blot analysis. We found the weight of bodies and tissues (retroperitoneal fat pads, kidneys and livers) of mice fed with HFD + BBD were significantly lower than that of HFD-fed mice. And liver injury induced by HFD was relieved in mice treated with BBD, accompanied with significant reduction were observed in serum ALT/AST activities and alleviated pathological damage. The levels of glucose, TG, TC, HDL-C and LDL-C in the liver or serum were significantly decreased on HFD + BBD group compared with HFD group. Furthermore, BBD treatment reduced the level of TNF-[alpha] and IL-6 induced by HFD. The level of leptin in the liver and serum were reduced in mice fed with HFD + BBD than that of HFD-fed mice. Several lipid synthesis genes (SREBP1-c, ACC, SCD-1, LXR[alpha] and CD36) were down-regulated and that of ss-oxidation (CPT-1 and PPAR[alpha]) up-regulated in HFD + BBD group compared with HFD group. In addition, BBD increased the expression of p-AMPK compared with untreated HFD group, which suggested BBD improved the activation of AMPK pathway. In summary, our results indicate that BBD has potential applications in the prevention and treatment of NAFLD, which may be closely related to its effect on lipid metabolism via activation of AMPK signaling. Babaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease progression, but little is known about its effect on non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the effects of BBD on obesity-induced NAFLD.BACKGROUNDBabaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease progression, but little is known about its effect on non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the effects of BBD on obesity-induced NAFLD.C57BL/6 J mice were fed with normal diet, high fat diet (HFD) or HFD + BBD for 8 weeks. Weights of all mice were recorded every 3 days. At the end of the experiments, the level of livers, kidneys and adipose tissues of each animal was weighed. Blood serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) cholesterol, low density lipoprotein cholesterol (LDL-C), glucose and leptin were detected with appropriate test kits. Haematoxylin-eosin (HE), Masson trichrome and Oil Red O staining of the liver were performed. We applied immunohistochemical analysis to investigate the expression of TNF-α, IL-6 and leptin in liver tissue. The expression of genes related lipid anabolism (SREBP1-c, ACC, SCD-1, LXRα and CD36) and ß-oxidation (CPT-1 and PPARα) in liver and adipose tissues was determined by RT-PCR. The expression of AMPK and p-AMPK was determined by western blot analysis.METHODSC57BL/6 J mice were fed with normal diet, high fat diet (HFD) or HFD + BBD for 8 weeks. Weights of all mice were recorded every 3 days. At the end of the experiments, the level of livers, kidneys and adipose tissues of each animal was weighed. Blood serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) cholesterol, low density lipoprotein cholesterol (LDL-C), glucose and leptin were detected with appropriate test kits. Haematoxylin-eosin (HE), Masson trichrome and Oil Red O staining of the liver were performed. We applied immunohistochemical analysis to investigate the expression of TNF-α, IL-6 and leptin in liver tissue. The expression of genes related lipid anabolism (SREBP1-c, ACC, SCD-1, LXRα and CD36) and ß-oxidation (CPT-1 and PPARα) in liver and adipose tissues was determined by RT-PCR. The expression of AMPK and p-AMPK was determined by western blot analysis.We found the weight of bodies and tissues (retroperitoneal fat pads, kidneys and livers) of mice fed with HFD + BBD were significantly lower than that of HFD-fed mice. And liver injury induced by HFD was relieved in mice treated with BBD, accompanied with significant reduction were observed in serum ALT/AST activities and alleviated pathological damage. The levels of glucose, TG, TC, HDL-C and LDL-C in the liver or serum were significantly decreased on HFD + BBD group compared with HFD group. Furthermore, BBD treatment reduced the level of TNF-α and IL-6 induced by HFD. The level of leptin in the liver and serum were reduced in mice fed with HFD + BBD than that of HFD-fed mice. Several lipid synthesis genes (SREBP1-c, ACC, SCD-1, LXRα and CD36) were down-regulated and that of ß-oxidation (CPT-1 and PPARα) up-regulated in HFD + BBD group compared with HFD group. In addition, BBD increased the expression of p-AMPK compared with untreated HFD group, which suggested BBD improved the activation of AMPK pathway.RESULTSWe found the weight of bodies and tissues (retroperitoneal fat pads, kidneys and livers) of mice fed with HFD + BBD were significantly lower than that of HFD-fed mice. And liver injury induced by HFD was relieved in mice treated with BBD, accompanied with significant reduction were observed in serum ALT/AST activities and alleviated pathological damage. The levels of glucose, TG, TC, HDL-C and LDL-C in the liver or serum were significantly decreased on HFD + BBD group compared with HFD group. Furthermore, BBD treatment reduced the level of TNF-α and IL-6 induced by HFD. The level of leptin in the liver and serum were reduced in mice fed with HFD + BBD than that of HFD-fed mice. Several lipid synthesis genes (SREBP1-c, ACC, SCD-1, LXRα and CD36) were down-regulated and that of ß-oxidation (CPT-1 and PPARα) up-regulated in HFD + BBD group compared with HFD group. In addition, BBD increased the expression of p-AMPK compared with untreated HFD group, which suggested BBD improved the activation of AMPK pathway.In summary, our results indicate that BBD has potential applications in the prevention and treatment of NAFLD, which may be closely related to its effect on lipid metabolism via activation of AMPK signaling.CONCLUSIONIn summary, our results indicate that BBD has potential applications in the prevention and treatment of NAFLD, which may be closely related to its effect on lipid metabolism via activation of AMPK signaling. Babaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease progression, but little is known about its effect on non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the effects of BBD on obesity-induced NAFLD. C57BL/6 J mice were fed with normal diet, high fat diet (HFD) or HFD + BBD for 8 weeks. Weights of all mice were recorded every 3 days. At the end of the experiments, the level of livers, kidneys and adipose tissues of each animal was weighed. Blood serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) cholesterol, low density lipoprotein cholesterol (LDL-C), glucose and leptin were detected with appropriate test kits. Haematoxylin-eosin (HE), Masson trichrome and Oil Red O staining of the liver were performed. We applied immunohistochemical analysis to investigate the expression of TNF-α, IL-6 and leptin in liver tissue. The expression of genes related lipid anabolism (SREBP1-c, ACC, SCD-1, LXRα and CD36) and ß-oxidation (CPT-1 and PPARα) in liver and adipose tissues was determined by RT-PCR. The expression of AMPK and p-AMPK was determined by western blot analysis. We found the weight of bodies and tissues (retroperitoneal fat pads, kidneys and livers) of mice fed with HFD + BBD were significantly lower than that of HFD-fed mice. And liver injury induced by HFD was relieved in mice treated with BBD, accompanied with significant reduction were observed in serum ALT/AST activities and alleviated pathological damage. The levels of glucose, TG, TC, HDL-C and LDL-C in the liver or serum were significantly decreased on HFD + BBD group compared with HFD group. Furthermore, BBD treatment reduced the level of TNF-α and IL-6 induced by HFD. The level of leptin in the liver and serum were reduced in mice fed with HFD + BBD than that of HFD-fed mice. Several lipid synthesis genes (SREBP1-c, ACC, SCD-1, LXRα and CD36) were down-regulated and that of ß-oxidation (CPT-1 and PPARα) up-regulated in HFD + BBD group compared with HFD group. In addition, BBD increased the expression of p-AMPK compared with untreated HFD group, which suggested BBD improved the activation of AMPK pathway. In summary, our results indicate that BBD has potential applications in the prevention and treatment of NAFLD, which may be closely related to its effect on lipid metabolism via activation of AMPK signaling. Abstract Background Babaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease progression, but little is known about its effect on non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the effects of BBD on obesity-induced NAFLD. Methods C57BL/6 J mice were fed with normal diet, high fat diet (HFD) or HFD + BBD for 8 weeks. Weights of all mice were recorded every 3 days. At the end of the experiments, the level of livers, kidneys and adipose tissues of each animal was weighed. Blood serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) cholesterol, low density lipoprotein cholesterol (LDL-C), glucose and leptin were detected with appropriate test kits. Haematoxylin–eosin (HE), Masson trichrome and Oil Red O staining of the liver were performed. We applied immunohistochemical analysis to investigate the expression of TNF-α, IL-6 and leptin in liver tissue. The expression of genes related lipid anabolism (SREBP1-c, ACC, SCD-1, LXRα and CD36) and ß-oxidation (CPT-1 and PPARα) in liver and adipose tissues was determined by RT-PCR. The expression of AMPK and p-AMPK was determined by western blot analysis. Results We found the weight of bodies and tissues (retroperitoneal fat pads, kidneys and livers) of mice fed with HFD + BBD were significantly lower than that of HFD-fed mice. And liver injury induced by HFD was relieved in mice treated with BBD, accompanied with significant reduction were observed in serum ALT/AST activities and alleviated pathological damage. The levels of glucose, TG, TC, HDL-C and LDL-C in the liver or serum were significantly decreased on HFD + BBD group compared with HFD group. Furthermore, BBD treatment reduced the level of TNF-α and IL-6 induced by HFD. The level of leptin in the liver and serum were reduced in mice fed with HFD + BBD than that of HFD-fed mice. Several lipid synthesis genes (SREBP1-c, ACC, SCD-1, LXRα and CD36) were down-regulated and that of ß-oxidation (CPT-1 and PPARα) up-regulated in HFD + BBD group compared with HFD group. In addition, BBD increased the expression of p-AMPK compared with untreated HFD group, which suggested BBD improved the activation of AMPK pathway. Conclusion In summary, our results indicate that BBD has potential applications in the prevention and treatment of NAFLD, which may be closely related to its effect on lipid metabolism via activation of AMPK signaling. Background Babaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease progression, but little is known about its effect on non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the effects of BBD on obesity-induced NAFLD. Methods C57BL/6 J mice were fed with normal diet, high fat diet (HFD) or HFD + BBD for 8 weeks. Weights of all mice were recorded every 3 days. At the end of the experiments, the level of livers, kidneys and adipose tissues of each animal was weighed. Blood serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) cholesterol, low density lipoprotein cholesterol (LDL-C), glucose and leptin were detected with appropriate test kits. Haematoxylin–eosin (HE), Masson trichrome and Oil Red O staining of the liver were performed. We applied immunohistochemical analysis to investigate the expression of TNF-α, IL-6 and leptin in liver tissue. The expression of genes related lipid anabolism (SREBP1-c, ACC, SCD-1, LXRα and CD36) and ß-oxidation (CPT-1 and PPARα) in liver and adipose tissues was determined by RT-PCR. The expression of AMPK and p-AMPK was determined by western blot analysis. Results We found the weight of bodies and tissues (retroperitoneal fat pads, kidneys and livers) of mice fed with HFD + BBD were significantly lower than that of HFD-fed mice. And liver injury induced by HFD was relieved in mice treated with BBD, accompanied with significant reduction were observed in serum ALT/AST activities and alleviated pathological damage. The levels of glucose, TG, TC, HDL-C and LDL-C in the liver or serum were significantly decreased on HFD + BBD group compared with HFD group. Furthermore, BBD treatment reduced the level of TNF-α and IL-6 induced by HFD. The level of leptin in the liver and serum were reduced in mice fed with HFD + BBD than that of HFD-fed mice. Several lipid synthesis genes (SREBP1-c, ACC, SCD-1, LXRα and CD36) were down-regulated and that of ß-oxidation (CPT-1 and PPARα) up-regulated in HFD + BBD group compared with HFD group. In addition, BBD increased the expression of p-AMPK compared with untreated HFD group, which suggested BBD improved the activation of AMPK pathway. Conclusion In summary, our results indicate that BBD has potential applications in the prevention and treatment of NAFLD, which may be closely related to its effect on lipid metabolism via activation of AMPK signaling. |
ArticleNumber | 77 |
Audience | Academic |
Author | Li, Rong Gao, Lu Zhang, Li Zhao, Naping Zhao, Shanmin Hou, Jing Wei, Lixin Zheng, Huifei Ye, Fei Jin, Yuxiang Zhao, Qiudong Sheng, Dandan Han, Zhipeng Liu, Wenting |
Author_xml | – sequence: 1 givenname: Dandan surname: Sheng fullname: Sheng, Dandan – sequence: 2 givenname: Shanmin surname: Zhao fullname: Zhao, Shanmin – sequence: 3 givenname: Lu surname: Gao fullname: Gao, Lu – sequence: 4 givenname: Huifei surname: Zheng fullname: Zheng, Huifei – sequence: 5 givenname: Wenting surname: Liu fullname: Liu, Wenting – sequence: 6 givenname: Jing surname: Hou fullname: Hou, Jing – sequence: 7 givenname: Yuxiang surname: Jin fullname: Jin, Yuxiang – sequence: 8 givenname: Fei surname: Ye fullname: Ye, Fei – sequence: 9 givenname: Qiudong surname: Zhao fullname: Zhao, Qiudong – sequence: 10 givenname: Rong surname: Li fullname: Li, Rong – sequence: 11 givenname: Naping surname: Zhao fullname: Zhao, Naping – sequence: 12 givenname: Li surname: Zhang fullname: Zhang, Li – sequence: 13 givenname: Zhipeng surname: Han fullname: Han, Zhipeng – sequence: 14 givenname: Lixin orcidid: 0000-0002-6383-7452 surname: Wei fullname: Wei, Lixin |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31548878$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1016/S0140-6736(14)60460-8 10.1172/JCI23621 10.1007/s11655-017-2279-1 10.18632/oncotarget.12783 10.2337/db06-1076 10.1172/JCI6223 10.1056/NEJMc1710026 10.3748/wjg.v25.i2.163 10.1016/j.cytogfr.2018.10.002 10.2337/db13-0670 10.1038/sj.ijo.0802502 10.1016/S1499-3872(14)60024-2 10.1113/jphysiol.2006.111484 10.1038/nrdp.2017.34 10.1038/nrn.2016.24 10.1267/ahc.13005 10.1007/s00125-017-4523-9 10.1016/j.bbadis.2017.08.026 10.1096/fj.04-2204com 10.1042/CS20160136 10.1074/jbc.M112.347211 10.1074/jbc.M202638200 10.1007/s00125-014-3273-1 10.3748/wjg.v21.i18.5695 10.1142/S0192415X18500076 10.1038/415339a 10.1152/ajpgi.00456.2009 10.3389/fmicb.2017.02010 10.1016/j.cmet.2011.03.009 10.1093/cvr/cvp118 10.1152/physrev.00038.2012 10.1002/hep.28431 10.1007/s00125-015-3769-3 |
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Keywords | Lipid metabolism AMPK pathway Non-alcoholic fatty liver disease Babaodan |
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References | SA Polyzos (339_CR9) 2016; 59 Y Minokoshi (339_CR12) 2002; 415 M Wang (339_CR29) 2017; 1863 X Deng (339_CR24) 2012; 287 Z Shen (339_CR36) 2010; 298 FB Ortega (339_CR2) 2017; 377 L Liang (339_CR8) 2016; 7 M Wang (339_CR25) 2018; 1 M Ng (339_CR5) 2014; 384 K Clement (339_CR15) 2004; 18 AK Stoeckman (339_CR27) 2002; 277 L Zhang (339_CR19) 2014; 13 TT Wang (339_CR20) 2018; 44 S Kersten (339_CR32) 1999; 103 N Tanaka (339_CR3) 2019; 25 HM O’Neill (339_CR10) 2014; 57 H Han (339_CR28) 2017; 2017 EA Richter (339_CR33) 2013; 93 KL Donnelly (339_CR13) 2005; 115 CN Lumeng (339_CR14) 2007; 56 339_CR17 M Nakazawa (339_CR23) 2013; 46 CC Alves (339_CR31) 2017; 8 Y Li (339_CR35) 2011; 13 K Bujold (339_CR30) 2009; 83 M Pigeyre (339_CR22) 2016; 130 W He (339_CR18) 2018; 61 GS Hotamisligil (339_CR16) 2003; 27 R Zachariah Tom (339_CR26) 2014; 63 P Gonzalez-Muniesa (339_CR1) 2017; 3 S Nepali (339_CR11) 2018; 46 ZM Younossi (339_CR4) 2016; 64 JZ Zhu (339_CR6) 2015; 21 B Xu (339_CR21) 2016; 17 M Daval (339_CR34) 2006; 574 LB Song (339_CR7) 2017; 23 |
References_xml | – volume: 384 start-page: 766 year: 2014 ident: 339_CR5 publication-title: Lancet. doi: 10.1016/S0140-6736(14)60460-8 – volume: 2017 start-page: 3256241 year: 2017 ident: 339_CR28 publication-title: Oxid Med Cell Longev. – volume: 115 start-page: 1343 year: 2005 ident: 339_CR13 publication-title: J Clin Invest. doi: 10.1172/JCI23621 – volume: 1 start-page: 1 year: 2018 ident: 339_CR25 publication-title: Crit Rev Food Sci Nutr. – volume: 23 start-page: 937 year: 2017 ident: 339_CR7 publication-title: Chin J Integr Med. doi: 10.1007/s11655-017-2279-1 – volume: 7 start-page: 82554 year: 2016 ident: 339_CR8 publication-title: Oncotarget. doi: 10.18632/oncotarget.12783 – volume: 56 start-page: 16 year: 2007 ident: 339_CR14 publication-title: Diabetes doi: 10.2337/db06-1076 – volume: 103 start-page: 1489 year: 1999 ident: 339_CR32 publication-title: J Clin Invest. doi: 10.1172/JCI6223 – ident: 339_CR17 – volume: 377 start-page: 1495 year: 2017 ident: 339_CR2 publication-title: N Engl J Med doi: 10.1056/NEJMc1710026 – volume: 25 start-page: 163 year: 2019 ident: 339_CR3 publication-title: World J Gastroenterol doi: 10.3748/wjg.v25.i2.163 – volume: 44 start-page: 38 year: 2018 ident: 339_CR20 publication-title: Cytokine Growth Factor Rev doi: 10.1016/j.cytogfr.2018.10.002 – volume: 63 start-page: 1560 year: 2014 ident: 339_CR26 publication-title: Diabetes doi: 10.2337/db13-0670 – volume: 27 start-page: S53 issue: Suppl 3 year: 2003 ident: 339_CR16 publication-title: Int J Obes Relat Metab Disord doi: 10.1038/sj.ijo.0802502 – volume: 13 start-page: 138 year: 2014 ident: 339_CR19 publication-title: Hepatobiliary Pancreat Dis Int. doi: 10.1016/S1499-3872(14)60024-2 – volume: 574 start-page: 55 year: 2006 ident: 339_CR34 publication-title: J Physiol doi: 10.1113/jphysiol.2006.111484 – volume: 3 start-page: 17034 year: 2017 ident: 339_CR1 publication-title: Nat Rev Dis Primers. doi: 10.1038/nrdp.2017.34 – volume: 17 start-page: 282 year: 2016 ident: 339_CR21 publication-title: Nat Rev Neurosci doi: 10.1038/nrn.2016.24 – volume: 46 start-page: 75 year: 2013 ident: 339_CR23 publication-title: Acta Histochem Cytochem doi: 10.1267/ahc.13005 – volume: 61 start-page: S256 year: 2018 ident: 339_CR18 publication-title: Diabetologia doi: 10.1007/s00125-017-4523-9 – volume: 1863 start-page: 3190 year: 2017 ident: 339_CR29 publication-title: Biochim Biophys Acta Mol Basis Dis. doi: 10.1016/j.bbadis.2017.08.026 – volume: 18 start-page: 1657 year: 2004 ident: 339_CR15 publication-title: FASEB J. doi: 10.1096/fj.04-2204com – volume: 130 start-page: 943 year: 2016 ident: 339_CR22 publication-title: Clin Sci (Lond). doi: 10.1042/CS20160136 – volume: 287 start-page: 20132 year: 2012 ident: 339_CR24 publication-title: J Biol Chem. doi: 10.1074/jbc.M112.347211 – volume: 277 start-page: 27029 year: 2002 ident: 339_CR27 publication-title: J Biol Chem doi: 10.1074/jbc.M202638200 – volume: 57 start-page: 1693 year: 2014 ident: 339_CR10 publication-title: Diabetologia doi: 10.1007/s00125-014-3273-1 – volume: 21 start-page: 5695 year: 2015 ident: 339_CR6 publication-title: World J Gastroenterol doi: 10.3748/wjg.v21.i18.5695 – volume: 46 start-page: 119 year: 2018 ident: 339_CR11 publication-title: Am J Chin Med doi: 10.1142/S0192415X18500076 – volume: 415 start-page: 339 year: 2002 ident: 339_CR12 publication-title: Nature doi: 10.1038/415339a – volume: 298 start-page: G364 year: 2010 ident: 339_CR36 publication-title: Am J Physiol Gastrointest Liver Physiol doi: 10.1152/ajpgi.00456.2009 – volume: 8 start-page: 2010 year: 2017 ident: 339_CR31 publication-title: Front Microbiol. doi: 10.3389/fmicb.2017.02010 – volume: 13 start-page: 376 year: 2011 ident: 339_CR35 publication-title: Cell Metab doi: 10.1016/j.cmet.2011.03.009 – volume: 83 start-page: 457 year: 2009 ident: 339_CR30 publication-title: Cardiovasc Res doi: 10.1093/cvr/cvp118 – volume: 93 start-page: 993 year: 2013 ident: 339_CR33 publication-title: Physiol Rev doi: 10.1152/physrev.00038.2012 – volume: 64 start-page: 73 year: 2016 ident: 339_CR4 publication-title: Hepatology doi: 10.1002/hep.28431 – volume: 59 start-page: 30 year: 2016 ident: 339_CR9 publication-title: Diabetologia doi: 10.1007/s00125-015-3769-3 |
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Snippet | Babaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease progression, but... Background Babaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease... Abstract Background Babaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease... |
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SubjectTerms | Adipose tissue Alanine Alanine transaminase AMPK pathway Antigens Asian medicine Aspartate aminotransferase Babaodan Biological products Carbohydrates CD36 antigen Cholesterol Cholesterol tests Complications and side effects Diet Diet therapy Experiments Fatty liver Genes Glucose High density lipoprotein High fat diet Interleukin 6 Kidneys Laboratory animals Leptin Lipid metabolism Liver cancer Liver diseases Low density lipoprotein Low density lipoproteins Medical research Non-alcoholic fatty liver disease Obesity Oxidation Oxidation-reduction reactions Polymerase chain reaction Proteins Risk factors Serum levels Traditional Chinese medicine Triglycerides Tumor necrosis factor-TNF Tumor necrosis factor-α |
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Title | BabaoDan attenuates high-fat diet-induced non-alcoholic fatty liver disease via activation of AMPK signaling |
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