Korean red ginseng and its primary ginsenosides inhibit ethanol-induced oxidative injury by suppression of the MAPK pathway in TIB-73 cells

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• 作者：Hye-Min Park^a ; ^b ; ¹ ; Shang-Jin Kim^a ; ^b ; ^c ; ¹ ; A-Reum Mun^b ; Hyeon-Kyu Go^a ; ^b ; Gi-Beum Kim^a ; ^b ; ^c ; Sung-Zoo Kim^b ; Seon-Il Jang^d ; Sei-Jin Lee^e ; Jin-Shang Kim^a ; ^c ; Hyung-Sub Kang^a ; ^b ; ^c ; ^{kang-hs@jbnu.ac.kr}
• 关键词：Ethanol ; Ginsenoside Rg3 ; Ginsenoside Rh2 ; Hepatocyte ; Oxidative injury ; MAPK
• 刊名：Journal of Ethnopharmacology
• 出版年：2012
• 期刊代码：26_03788741
• 类别：pha
• 出版时间：14 June, 2012
• 卷：141
• 期：3
• 页码：1071-1076
• 文件大小：929 K

摘要

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Abstracts

Ethnopharmacological relevance

Panax ginseng (P. ginseng) is one of the most widely used medicinal plants due to its wide spectrum of medicinal effects. Among the currently available Panax ginseng products, Korea red ginseng (KRG) has been shown to exhibit a variety of antioxidative and hepatoprotective action.

Aim of the study

Our aim was to investigate the effects of KRG and its primary ginsenosides (Rg3 and Rh2) on EtOH-induced injury to mouse hepatocytes (TIB-73).

Materials and methods

We investigated the effects of KRG and its primary ginsenoside on EtOH-induced injury to TIB-73 cells and evaluated MAPKs signals as a possible mechanism of action. Hepatocytic injury was evaluated by biochemical assays as cell viability, lactate dehydrogenase (LDH), aspartate aminotransferase (AST), ROS and mitochondria membrane potential (MMP) level in TIB-73 cells. The levels of MAPK activation were analyzed by Western blots.

Results

The results showed that exposure of EtOH to TIB-73 cells led to cell death and membrane damage, accompanied by a decrease in cell viability, MMP, and Mg²⁺ concentrations, but an increase in LDH, AST, ROS and MAPK activation. KRG and its primary ginsenosides reduced EtOH-induced generation of ROS and the activation of ERK and JNK, and increased Mg²⁺ concentrations.

Conclusion

These results suggest that KRG and its primary ginsenosides inhibit EtOH-induced oxidative injury by suppression of the MAPK pathway in TIB-73 cells.