Protective Effects of Ginsenoside Rb1 on Septic Rats and Its Mechanism

作     者：WU Li Li JIA Bao Hui SUN Jian CHEN Jun Xi LIU Zhong Ying LIU Yuan 

作者机构：Department of Emergency and ICU Fourth Affiliated Hospital of Nanchang University School of Life Sciences and Food Engineering Nanchang University 

出 版 物：《Biomedical and Environmental Sciences》 (生物医学与环境科学（英文版）)

年 卷 期：2014年第27卷第4期

页      面：300-303页

核心收录：

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

基　　金：supported by the Major Invite Tender Project of Health Department of Jiangxi Province(No.20104005) the Major Project of the Department of Education of Jiangxi Province(No.GJJ12003) the 13th’Challenge Cup’of Extracurricular academic and scientific works of Nanchang University 

主　　题：Rb CLP Protective Effects of Ginsenoside Rb1 on Septic Rats and Its Mechanism 

摘      要：This study aims to observe the protective effects of ginsenoside Rbl on liver and lung in rats with septic shock and reveal its mechanism. Rats were randomly divided into three groups： sham, cecal ligation and puncture （CLP）, and CLP with ginsenoside Rb1. Then, the survival rate, arterial blood pressure, TLR4 mRNA, and TNF-α levels were determined. The liver and lung tissues were stained with hematoxylin-eosin （HE）. The overall survival rate of the Rb1 group was significantly higher than that of the CLP group. Mean arterial blood pressure went down in both the CLP and Rb1 groups after CLP, and there was a significant difference both in the sham and Rb1 groups when compared with the CLP group. The Rb1 treatment group had markedly lower TLR4 mRNA expression and TNF-a levels than the CLP group. In the CLP group, pathology showed swelling, degeneration, necrosis, and neutrophii infiltration in the liver and alveolar epithelial cells. However, in the Rb1 group, there was mild degeneration and slight neutrophil infiltration, but no obvious necrosis. Rb1 may improve the survival rate, ameliorate arterial blood pressure, and protect the liver and lung in septic shock rats by downregulating the expression of TLR4 mRNA and inhibiting the production of TNF-α.