Ginsenoside Rg1 attenuates concanavalin A-induced hepatitis in mice through inhibition of cytokine secretion and lymphocyte infiltration

被引:5
作者
Lijun Cao
Yun Zou
Jiali Zhu
Xiaohua Fan
Jinbao Li
机构
[1] Second Military Medical University,Department of Anesthesiology and Intensive Care, Changhai Hospital
来源
Molecular and Cellular Biochemistry | 2013年 / 380卷
关键词
Ginsenoside Rg1; Concanavalin A; Hepatitis; Lymphocyte;
D O I
暂无
中图分类号
学科分类号
摘要
The effect of ginsenoside Rg1 (Rg1) on hepatic damage caused by concanavalin A (Con A) has not been fully elucidated. This study was designed to evaluate the protective effect of Rg1 on Con A-induced hepatitis in mice and explore the potential mechanisms of this effect. C57BL/6 mice were divided randomly into the following four experimental groups: phosphate-buffered saline group, Rg1 group, Con A group, Con A + Rg1 group. Mice received Rg1 (20 mg/kg) 3 h before intravenous administration of Con A (15 mg/kg). Levels of alanine transaminase, aspartate transaminase and cytokine production were measured, the amount of phosphorylated IκBα and p65 were tested, the numbers of CD4+ and CD8+ T lymphocytes infiltrated in the blood, spleen and liver were calculated, intercellular adhesion molecule-1 (ICAM-1) and interferon-inducible chemokine-10 (CXCL-10) levels were measured and histological examination of the livers was conducted. Pretreatment with Rg1 markedly reduced the elevated levels of serum aminotransferase, ameliorated liver damage and suppressed proinflammatory cytokines secretion via inhibition NF-κB activity following Con A injection of mice. Furthermore, Rg1 administration reduced ICAM-1 and CXCL-10 mRNA expression in the liver as well as the number of CD4+ and CD8+ T lymphocytes infiltrating in the liver. Rg1 reduced the incidence of liver damage through inhibition of the proinflammatory response and suppressed the recruitment of CD4+ and CD8+ T lymphocytes to the liver. These data indicate that Rg1 represents a novel agent for the treatment of T lymphocyte-dependent liver injury.
引用
收藏
页码:203 / 210
页数:7
相关论文
共 195 条
[1]  
Watanabe S(2010)Suppression of Con A-induced hepatitis induction in ICOS-deficient mice Immunol Lett 128 51-58
[2]  
Ohnuki K(1992)A T cell-dependent experimental liver injury in mice inducible by concanavalin A J Clin Invest 90 196-203
[3]  
Hara Y(2007)Baicalin protects mouse from concanavalin A-induced liver injury through inhibition of cytokine production and hepatocyte apoptosis Liver Int 27 582-591
[4]  
Ishida Y(2005)Induction of thymocyte apoptosis by systemic administration of concanavalin A in mice: role of TNF-alpha, IFN-gamma and glucocorticoids Eur J Immunol 35 2304-2312
[5]  
Ikarashi Y(2002)Opposing roles of STAT1 and STAT3 in T cell-mediated hepatitis: regulation by SOCS J Clin Invest 110 1503-1513
[6]  
Ogawa S(2012)Immune mechanisms of concanavalin A model of autoimmune hepatitis World J Gastroenterol 18 119-125
[7]  
Kishimoto H(2006)L-selectin and intercellular adhesion molecule-1 regulate the development of concanavalin A-induced liver injury J Leukoc Biol 79 696-705
[8]  
Tanabe K(2008)Lymphocyte recruitment to the liver: molecular insights into the pathogenesis of liver injury and hepatitis Toxicology 254 136-146
[9]  
Abe R(2001)TNF-alpha-induced expression of adhesion molecules in the liver is under the control of TNFR1—relevance for concanavalin A-induced hepatitis J Immunol 166 1300-1307
[10]  
Tiegs G(2004)IFN-gamma/STAT1 acts as a proinflammatory signal in T cell-mediated hepatitis via induction of multiple chemokines and adhesion molecules: a critical role of IRF-1 Am J Physiol Gastrointest Liver Physiol 287 G1044-G1052