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Aristolochia manshuriensis Kom ethyl acetate extract protects against high-fat diet-induced non-alcoholic steatohepatitis by regulating kinase phosphorylation in mouse

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Related in: MedlinePlus

Effects of EtOAc extract of AMK on hepatic TG and lipoperoxide content in NASH mice. (A) Hepatic TG and (B) lipoperoxide content were assessed in mice fed ND, HFD, or HFD treated with EtOAc extract of AMK (2.5 mg/kg) for 12 weeks. Data are the means ± SD of 10 mice in each group. *p < 0.05 vs. HFD-fed mice. SOD, superoxide dismutase; GPx, glutathione peroxidase; GR, glutathione reductase; GSH, glutathione; TBARS, thiobarbituric acid reactive substances.
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Figure 3: Effects of EtOAc extract of AMK on hepatic TG and lipoperoxide content in NASH mice. (A) Hepatic TG and (B) lipoperoxide content were assessed in mice fed ND, HFD, or HFD treated with EtOAc extract of AMK (2.5 mg/kg) for 12 weeks. Data are the means ± SD of 10 mice in each group. *p < 0.05 vs. HFD-fed mice. SOD, superoxide dismutase; GPx, glutathione peroxidase; GR, glutathione reductase; GSH, glutathione; TBARS, thiobarbituric acid reactive substances.

Mentions: Consumption of HFD increased TG (panel A in Fig. 3) and TBARS (panel B in Fig. 3) levels compared with the ND mice. However, treatment with the EtOAc extract markedly inhibited these increases. In the hepatocytes of mice treated with EtOAc extract of AMK (2.5 mg/kg), the levels of both TG and TBARS was significantly decreased compared to mice fed with the HFD alone (Fig. 3).


Aristolochia manshuriensis Kom ethyl acetate extract protects against high-fat diet-induced non-alcoholic steatohepatitis by regulating kinase phosphorylation in mouse
Effects of EtOAc extract of AMK on hepatic TG and lipoperoxide content in NASH mice. (A) Hepatic TG and (B) lipoperoxide content were assessed in mice fed ND, HFD, or HFD treated with EtOAc extract of AMK (2.5 mg/kg) for 12 weeks. Data are the means ± SD of 10 mice in each group. *p < 0.05 vs. HFD-fed mice. SOD, superoxide dismutase; GPx, glutathione peroxidase; GR, glutathione reductase; GSH, glutathione; TBARS, thiobarbituric acid reactive substances.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037294&req=5

Figure 3: Effects of EtOAc extract of AMK on hepatic TG and lipoperoxide content in NASH mice. (A) Hepatic TG and (B) lipoperoxide content were assessed in mice fed ND, HFD, or HFD treated with EtOAc extract of AMK (2.5 mg/kg) for 12 weeks. Data are the means ± SD of 10 mice in each group. *p < 0.05 vs. HFD-fed mice. SOD, superoxide dismutase; GPx, glutathione peroxidase; GR, glutathione reductase; GSH, glutathione; TBARS, thiobarbituric acid reactive substances.
Mentions: Consumption of HFD increased TG (panel A in Fig. 3) and TBARS (panel B in Fig. 3) levels compared with the ND mice. However, treatment with the EtOAc extract markedly inhibited these increases. In the hepatocytes of mice treated with EtOAc extract of AMK (2.5 mg/kg), the levels of both TG and TBARS was significantly decreased compared to mice fed with the HFD alone (Fig. 3).

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Related in: MedlinePlus