摘要
目的研究TNF-α和Th1/Th2型细胞因子(IFN-γ/IL-4)在D-氨基半乳糖/内毒素所致急性肝衰竭大鼠血清和肝、肺组织中的表达。方法取30只Wistar大鼠腹腔内注射D-氨基半乳糖/内毒素诱导大鼠急性肝衰竭模型(AHF组,n=30),于造模3、6、12、24、48、72h各取5只检测其血清丙氨酸转氨酶(ALT),肝组织的病理形态学变化,血清中TNF-α和IFN-γ/IL-4水平的变化,肝、肺组织内TNF-α和IFN-γ/IL-4的表达。另取30只Wistar大鼠腹腔内注射等量生理盐水为正常对照(N组,n=30)。结果AHF组各时间点血清ALT的增高和N组相比有统计学差异(P<0.05),肝内炎细胞浸润、坏死明显;AHF组血清内TNF-α3、6h分别为0.255±0.133、0.150±0.061,比N组相应时间点均增高(P<0.01,P<0.05);Th1型细胞因子(IFN-γ)与N组相比3、6h均增高(P均<0.01);Th2型细胞因子(IL-4)水平在各时间点无明显变化(P>0.05);AHF组肺组织与N组相比TNF-α的表达在3、6、12h均明显增高(P均<0.01)。结论TNF-α和IFN-γ在急性肝衰竭大鼠模型的早期阶段起重要作用;IL-4可能不参与此动物模型的病理过程;肺组织TNF-α增高与肝衰竭的关系值得探讨。
Objective To research the expression of TNF-α and Th1/Th2 cytokines （IFN-γ/IL-4） in sera, livers and lungs of D-glactosamine/endotoxin-induced acute hepatic failure rats. Methods Wistar rats with acute hepatic failure （AHF group, n = 30） were induced by intraperitoneal injection of D-glactosamine and endotoxin. To evaluate the hepatic injury,sera alanine transaminase（ALT） were determined and liver pathological morphology were observed at 3, 6,12,24,48 and 72 h following intraperitoneal injection of D-glactosamine and endotoxin. Simultaneously, sera TNF-α and IFN-γ/IL-4 were examined by ELISA. The expression of TNF-α and IFN-γ/IL-4 in livers and lungs were detected by immunohistochemistry techenique. Wistar rats were injected with physiological saline solution as normal controls （N group,n = 30）. Results Sera ALT increased significantly in AHF group than that in N group （P 〈 0.05 ） at all time points. Infiltration of inflammatory cells and necrosis of hepatic cells were obvious in AHF group. Compared with N group, levels of sera TNF-α in AHF group were obviously higher at 3 h（P 〈 0.01 ） and 6 h（P 〈 0.05 ）. And Th1 cyto- kine （IFN-γ） were obviously higher at 3 h（P 〈 0.01 ） and 6 h （ P 〈 0.01 ）. Th2 cytokine （IL-4） weren＇t obviously higher at all time points（ P 〉 0.05 ）. The expression of TNF-α in lungs in AHF group were markedly stronger than that in N group at 3 h,6 h and 12 h,respectively（P 〈 0.01 ）. Conclusion TNF-α and IFN-γ may play important role in the AHF models at early phase. However, IL-4 may not contribute to the AHF. It is worth researching the relation of AHF and the improvement of TNF-α＇s level of lungs.
出处
《胃肠病学和肝病学杂志》
CAS
2008年第6期500-502,共3页
Chinese Journal of Gastroenterology and Hepatology
基金
山西省自然科学基金(20011073)
