Saeng-Kankunbi-Tang(生肝健脾汤) Protects Liver against Oxidative Damage through Activation of ERK/Nrf2 Pathway

作     者：In Woo Lee Hee Yoon Choi Ju-Hee Lee Sun-Dong Park Seung Mo Kim Sae Kwang Ku 赵容杰 Sang Chan Kim Young Woo Kim Hong Sik Choi 

作者机构：Department of Internal Oriental Medicine of HepatologyCollege of Oriental Medicine Daegu Haany University Daegu 38610 Korea Medical Research Center for Globalization of Herbal Formulation College of Oriental Medicine Daegu Haany University Daegu 38610 Korea College of Oriental Medicine Dongguk University Gyeongju 38066 Korea School of Mental Health Jining Medical University JiningShandong Province 272067 China 

出 版 物：《Chinese Journal of Integrative Medicine》 (中国结合医学杂志（英文版）)

年 卷 期：2016年第22卷第8期

页      面：619-628页

核心收录：

学科分类：1008[医学-中药学(可授医学、理学学位)] 1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 1005[医学-中医学] 1002[医学-临床医学] 100602[医学-中西医结合临床] 10[医学] 

基　　金：Supported by the National Research Foundation of Korea Grant funded by the Korea government(No.2014R1A2A2A01007375 No.2012R1A5A2A42671316) 

主　　题：Saeng kankunbi tang mitochondria nuclear factor erythroid 2 related factor 2 oxidative stress liver mouse 

摘      要：Objective： To investigate the cytoprotective effects of Saeng-kankunbi-tang（生肝健脾汤, SKT）, a herbal prescription consisting of Artemisia capillaris and Alisma canaliculatum, and its underlying mechanism involved. Methods： In mice, blood biochemistry and histopathology were assessed in carbon tetrachloride（CCl4）-induced oxidative hepatic injury in vivo. The animal groups included vehicle-treated control, CCl4, SKT 500 mg/（kg·day） CCl4＋SKT 200 or 500 mg/（kg·day）. In Hep G2 cell, tert-butyl hydroperoxide（t BHP） induced severe oxidative stress and mitochondrial dysfunction in vitro. The cyto-protective effects of SKT were determined by 3-（4,5-dimethylthiazol）-2,5-diphenyltetrazolium bromide（MTT） assay, fluorescence activated cell sorting analysis and western blotting. Results： The administration of SKT prevented liver damage induced by CCl4 in mice, by inhibition of hepatocyte degeneration and inflammatory cell infiltration as well as plasma parameters such as alanine aminotransferase（P〈0.01）. Moreover, treatment with t BHP induced hepatocyte death and cellular reactive oxygen species production in hepatocyte cell line. However, SKT pretreatment（30–300 μg/m L） reduced this cell death and oxidative stress（P〈0.01）. More importantly, SKT inhibited the ability of t BHP to induce changes in mitochondrial membrane transition in cell stained with rhodamine 123（P〈0.01）. Furthermore, treatment with SKT induced extracellular signal-regulated kinases-mediated nuclear factor erythroid-2-related factor 2（Nrf2） activation as well as the expressions of heme oxygenase 1 and glutamate-cystein ligase catalytic, Nrf2 target genes. Conclusion： SKT has the ability to protect hepatocyte against oxidative stress and mitochondrial damage mediated by Nrf2 activation.