Aristolochia manshuriensis Kom ethyl acetate extract protects against high-fat diet-induced non-alcoholic steatohepatitis by regulating kinase phosphorylation in mouse.
10.4142/jvs.2016.17.3.279
- Author:
Dong Hoon KWAK
1
;
Ji Su KIM
;
Kyu Tae CHANG
;
Young Kug CHOO
Author Information
1. Institute for Glycoscience, College of Natural Sciences, Wonkwang University, Iksan 54538, Korea. ykchoo@wonkwang.ac.kr
- Publication Type:Original Article
- Keywords:
Aristolochia manshuriensis Kom;
c-jun N-terminal kinase 1/2;
extracellular signal-regulated kinase 1/2;
inflammation;
nonalcoholic steatohepatitis
- MeSH:
Animals;
Apoptosis;
Aristolochia*;
Diet, High-Fat;
Eating;
Fatty Liver*;
Hepatocytes;
Inflammation;
JNK Mitogen-Activated Protein Kinases;
Lipid Peroxidation;
Lipoproteins;
Liver;
Medicine, Traditional;
Mice*;
Non-alcoholic Fatty Liver Disease;
Phosphorylation*;
Phosphotransferases*;
Reactive Oxygen Species;
Therapeutic Uses;
Triglycerides
- From:Journal of Veterinary Science
2016;17(3):279-287
- CountryRepublic of Korea
- Language:English
-
Abstract:
Aristolochia manshuriensis Kom (AMK) is an herb used as a traditional medicine; however, it causes side effects such as nephrotoxicity and carcinogenicity. Nevertheless, AMK can be applied in specific ways medicinally, including via ingestion of low doses for short periods of time. Non-alcoholic steatohepatitis (NASH) induced the hepatocyte injury and inflammation. The protective effects of AMK against NASH are unclear; therefore, in this study, the protective effects of AMK ethyl acetate extract were investigated in a high-fat diet (HFD)-induced NASH model. We found decreased hepatic steatosis and inflammation, as well as increased levels of lipoproteins during AMK extract treatment. We also observed decreased hepatic lipid peroxidation and triglycerides, as well as suppressed hepatic expression of lipogenic genes in extract-treated livers. Treatment with extract decreased the activation of c-jun N-terminal kinase 1/2 (JNK1/2) and increased the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2). These results demonstrate that the protective effect of the extract against HFD-induced NASH occurred via reductions in reactive oxygen species production, inflammation suppression, and apoptosis related to the suppression of JNK1/2 activation and increased ERK1/2 phosphorylation. Taken together, these results indicate that that ethyl acetate extract of AMK has potential therapeutic effects in the HFD-induced NASH mouse model.
