清肝活血方及其拆方对酒精性肝损伤大鼠肿瘤坏死因子α表达的影响

Effects of Qinggan Huoxue Recipe and its separated recipes on the expression of tumor necrosis factor-α in rats with alcoholic liver injury

目的:观察清肝活血方及其拆方对酒精性肝损伤(alcoholic liver injury,ALI)大鼠肝脏肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)mRNA表达和血浆TNF-α含量的影响。方法:除空白组和四氯化碳(carbon tetrachloride,CCl4)组外,80只雄性Wistar大鼠采用复合因素复制ALI模型。造模4周后将模型大鼠随机分成模型组、清肝方组、活血方组和清肝活血方组。3治疗组予相应药物灌胃。灌胃2周后,检测血清丙氨酸氨基转移酶(alanine aminotransferase,ALT)、天冬氨酸氨基转移酶(aspartate aminotransferase,AST)活性;采用酶联免疫吸附测定法检测血浆TNF-α含量;留取肝脏标本进行苏木素-伊红染色;逆转录聚合酶链反应检测肝组织TNF-αmRNA表达。结果:清肝活血方及其拆方均可明显改善ALI大鼠肝脏脂肪变及肝脏炎症程度,清肝活血方优于清肝方。清肝活血方能显著降低模型大鼠血清ALT活性;清肝方、活血方和清肝活血方均可明显降低ALI大鼠血清AST活性,组间比较差异无统计学意义。活血方及清肝活血方能显著降低模型大鼠肝组织TNF-αmRNA表达和血浆TNF-α水平,清肝方作用不明显。结论:清肝活血方及活血方治疗ALI的作用机制可能与减少TNF-α的产生有关。

Objective： To study the effects of Qinggan Huoxue Rec medicine, and its separated recipes on the expression TNF-α content in rats with alcoholic liver injury （ALl）. pe （QGHXR）, the compound traditional Chinese herbal of tumor necrosis factor-α （TNF-α） mRNA and serum TNF-α content in rats with alcoholic liver injury（ALI）.Methods： One hundred male Wistar rats were randomly divided into normal control group （n = 10）, carbon tetrachloride （CCI4） group （n=10） and ALl group （n=80）. Rats in the ALl group were intragastrically administered mixed liquor twice a day and intraperitoneally injected with CCl4 twice a week for 6 weeks, rats in the normal control group were intragastrically administered normal saline, and rats in the CCl4 group were intraperitoneally injected with CCItt and olive oil twice a week continuously. Two rats in the ALl group were sacrificed for histological observation per week. After 4-week modeling, the rats in the ALl group were randomly divided into QGHXR group, Qinggan Recipe （QGR） group, Huoxue Recipe （HXR） group （15 rats in each group）, and the others belonged to the untreated group. After 2-week suitable drugs treatment, the activities of serum alanine aminotransferase （ALT） and aspartate aminotransferase （AST） were analyzed. Pathological changes in liver tissues were observed by HE staining. The content of plasma TNF-α was assayed by enzyme linked immunosorbent assay, and expression of TNF-α mRNA in the liver tissue was detected by reverse transcription polymerase chain reaction （RT-PCR）. Results, QGHXR and its separated recipes improved liver steatosis and inflammation, and in this regard, the QGHXR was superior to the QGR. QGHXR decreased the activity of serum ALT in rats with ALl, but QGR and HXR did not show significant effect in that. The three recipes decreased the activity of AST as compared with the untreated group, but there were no significant differences among the three treated groups. HXR and QGHXR down-regulated the expression of TNF-α mRNA in the liver tissue, but QGR did not show significant effect. HXR and QGHXR also decreased the content of plasma TNF-α, but QGR did not show significant effect in that. Conclusion： QGHXR and HXR may provide protection against ALl in rats through decreasing the production of TNF-α.