Limits...
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 NASH mice. (A) Serum levels of high-density lipoprotein (HDL), low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) in NASH mice. (B) alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) in mice with NASH. The levels were measured in mice fed with ND, HFD, or HFD plus EtOAc extract of AMK (2.5 mg/kg) for 15 weeks. Each group consists of 10 mice. Data are expressed as the means ± SD. *p < 0.05 vs. HFD-fed mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC5037294&req=5

Figure 2: Effects of EtOAc extract of AMK on NASH mice. (A) Serum levels of high-density lipoprotein (HDL), low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) in NASH mice. (B) alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) in mice with NASH. The levels were measured in mice fed with ND, HFD, or HFD plus EtOAc extract of AMK (2.5 mg/kg) for 15 weeks. Each group consists of 10 mice. Data are expressed as the means ± SD. *p < 0.05 vs. HFD-fed mice.

Mentions: Serum TG and TC levels in the ND, HFD, and EtOAc groups are shown panel B in Fig. 1. The administration of the EtOAc extract (2.5 mg/kg) markedly increased the serum TC and TG levels (p < 0. 05) compared to HFD-fed mice. Fig. 2A shows the effects of EtOAc extract on the serum lipoprotein profiles of mice. The EtOAc extract of AMK dramatically reduced the LDL concentration (33%, p < 0.05) relative to that of the HFD-fed mice, and the serum levels of HDL and very low-density lipoprotein (VLDL) improved by about 20% and 33%, respectively, in the EtOAc extract-treated mice relative to the HFD-fed mice (panel A in Fig. 2). Additionally, serum of mice treated with extract of AMK EtOAc had ALP, AST, and ALT enzyme levels 54%, 52%, and 56% higher (p < 0.05) than those of HFD-fed mice, respectively, implying that AMK protected against HFD-induced liver injury (panel B in Fig. 2).


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 NASH mice. (A) Serum levels of high-density lipoprotein (HDL), low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) in NASH mice. (B) alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) in mice with NASH. The levels were measured in mice fed with ND, HFD, or HFD plus EtOAc extract of AMK (2.5 mg/kg) for 15 weeks. Each group consists of 10 mice. Data are expressed as the means ± SD. *p < 0.05 vs. HFD-fed mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 2: Effects of EtOAc extract of AMK on NASH mice. (A) Serum levels of high-density lipoprotein (HDL), low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) in NASH mice. (B) alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) in mice with NASH. The levels were measured in mice fed with ND, HFD, or HFD plus EtOAc extract of AMK (2.5 mg/kg) for 15 weeks. Each group consists of 10 mice. Data are expressed as the means ± SD. *p < 0.05 vs. HFD-fed mice.
Mentions: Serum TG and TC levels in the ND, HFD, and EtOAc groups are shown panel B in Fig. 1. The administration of the EtOAc extract (2.5 mg/kg) markedly increased the serum TC and TG levels (p < 0. 05) compared to HFD-fed mice. Fig. 2A shows the effects of EtOAc extract on the serum lipoprotein profiles of mice. The EtOAc extract of AMK dramatically reduced the LDL concentration (33%, p < 0.05) relative to that of the HFD-fed mice, and the serum levels of HDL and very low-density lipoprotein (VLDL) improved by about 20% and 33%, respectively, in the EtOAc extract-treated mice relative to the HFD-fed mice (panel A in Fig. 2). Additionally, serum of mice treated with extract of AMK EtOAc had ALP, AST, and ALT enzyme levels 54%, 52%, and 56% higher (p < 0.05) than those of HFD-fed mice, respectively, implying that AMK protected against HFD-induced liver injury (panel B in Fig. 2).

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