TLR3基因缺陷的肝纤维化小鼠血生化指标、肝组织纤维化标志物及炎性因子变化

摘要

目的 分析Toll样受体3(TLR3)基因缺陷的肝纤维化小鼠血生化指标、肝组织纤维化标志物及炎性因子变化.方法 将18只野生型雄性小鼠随机分为空白造模组和空白对照组,两组各9只;将18只TLR3基因缺陷型雄性小鼠随机分为TLR3造模组和TLR3对照组,两组各9只.空白造模组和TLR3造模组均注射四氯化碳,而空白对照组与TLR3对照组均注射玉米油.造模2个月后,采集血液标本,通过全自动生化分析仪对血清白蛋白(ALB)、总胆红素(TBIL)、天门冬氨酸氨基转移酶(AST)及丙氨酸氨基转移酶(ALT)水平进行测定.比较各组小鼠肝组织纤维化标志物(Ⅰ型胶原)表达水平和肝组织炎性因子如白介素6(IL-6)、肿瘤坏死因子-α(TNF-α)、单核细胞趋化因子-1(MCP-1)的表达水平.结果 空白造模组ALB水平较空白对照组明显降低,TBIL、AST及ALT等血生化指标的水平较空白对照组均显著升高(P0.05).空白造模组肝组织纤维化标志物(Ⅰ型胶原)表达水平较空白对照组显著升高(P0. 05). The expression level of hepatic fibrosis markers (type I collagen)in blank model group was significantly higher than that in blank control group (P < 0. 01),and the expression level of type I collagen in TLR3 model group was significantly higher than that of the blank model group and TLR3 control group (P < 0. 01). The expression levels of inflammatory factors such as IL - 6,TNF - α and MCP - 1 in liver tissue of blank model group were significantly higher than those in blank control group (P < 0. 05),and the levels of inflammatory factors in the TLR3 model group were significantly higher than those in the blank model group and TLR3 control group (P < 0. 05). Conclusion Type I collagen of liver fibrosis level increase significantly in TLR3 gene deficiency mice with liver fibrosis by carbon tetrachloride induced,and hepatic inflammatory fac-tors such as IL - 6,TNF - α and MCP - 1 expression also increase significantly,suggesting that TLR3 may be a protective gene,plays an impor-tant role in liver tissue block inflammatory factor in the occurrence and development of hepatic fibrosis.