摘要
目的探讨表没食子儿茶素没食子酸酯(EGCG)对ConA诱导的小鼠肝损伤的保护作用及其作用机制。方法 40只小鼠随机分为正常对照组、EGCG对照组、ConA模型组及EGCG+ConA组。采用HE法检测小鼠肝脏形态学改变,ELISA法检测血清ALT、AST的变化,采用免疫组化方法和Western blot方法检测各组小鼠肝组织中TNF-α与IL-17的变化。结果 ConA模型组ALT、AST的含量比对照组明显升高(<0.05),EGCG对照组与正常对照组比较无变化(>0.05),EGCG+ConA组比ConA模型组含量下降(<0.05)。ConA模型组小鼠肝脏显示较多肝细胞坏死,正常对照组和EGCG对照组小鼠肝脏正常,EGCG+ConA组肝细胞炎症坏死程度较ConA模型组有所减轻。ConA模型组小鼠肝组织中TNF-α与IL-17水平较正常对照组和EGCG对照组明显升高(<0.05),EGCG对照组与正常对照组比较无明显差异(>0.05),EGCG+ConA组比ConA模型组下降(<0.05)。结论 EGCG对ConA所致小鼠肝损伤有明显的保护作用,机制可能与其对炎性因子TNF-α与IL-17的调节有关。
Objective To explore the protective effect and its mechanism of EGCG in the injuried liver of mice caused by ConA. Methods 40 mice were randomly divided into normal control group, EGCG control group, ConA group and ConA+ EGCG group. The morphological change of mouse liver was detected by HE staining, the contents of ALT and AST in serum were determined by ELISA, the expressions of TNF-α and IL-17 in liver tissue were detected by immunohistocbemistry and Western blot. Results The contents of ALT and AST in serum were higher in ConA group than in normal control and EGCG control groups(P 〈0.05), without difference between normal control and EGCG control, but lower in ConA+ EGCG group than in ConA group(P〈0.05). Furthermore, EC, CG can also decrease the liver necrosis caused by ConA, and suppress the expressions of pro-inflammatory cytokines TNF- α and IL-17 in liver tissue. Conclusion The protective effect of EGCG on hepatic impairment might be related to the inhibition of TNF-α and IL- 17.
出处
《解剖科学进展》
CAS
2014年第3期229-232,共4页
Progress of Anatomical Sciences