【摘要】 目的观察肝缺血再灌注(I/R)损伤时诱导型一氧化氮合酶(iNOS)在肝组织中的表达及与肝细胞凋亡的关系,探讨其可能的机制。方法选健康雄性Wistar大鼠48只,随机分为假手术组、缺血30min组(I组)、缺血30min即刻再灌注组(I/R组)、缺血30min再灌注后1h组(I/R1h)、缺血30min再灌注后2h组(I/R2h)、缺血30min再灌注后4h组(I/R4h),每组8只。分别测定各组谷丙转氨酶(GTP)、碱性磷酸酶、γ-谷氨酰转肽酶含量及观察肝脏组织HE染色,应用免疫组化法分别测定各组大鼠iNOS在肝组织的表达,应用原位细胞凋亡法测定肝细胞凋亡。结果肝脏I/R过程导致了肝脏明显的损伤,表现为肝血清酶升高(P<0.01),肝细胞水肿,炎性细胞浸润,甚至有细胞坏死。病理组织学变化与GTP变化一致。肝组织iNOS在I/R组即有表达增高(P<0.01),I/R组与I组、I/R1h组与I/R组相比有统计学差异(P<0.05)。细胞凋亡指数I/R组与假手术组比较明显增加(P<0.01),I/R组与I组,I/R2h组与I/R1h组、I/R4h组与I/R2h组相比均有统计学差异(P<0.01)。iNOS与肝细胞凋亡指数间存在显著正相关(r=0.952),P<0.01)。结论肝脏I/R损伤可引起肝组织损伤及肝细胞凋亡,肝细胞的凋亡与iNOS的高表达有关。更多还原

【Abstract】 Objective To study the relationship between the expression of inducible nitric oxide synthase (iNOS) and liver cellular apoptosis following liver ischemia/reperfusion(I/R) injury in rats.Methods A model of liver I/R injury was established by imitation.Forty eight male Wistar rats were randomly divided into 6 groups: sham operation,ischemia 30min without reperfusion(group I),reperfusion following ischemia-30min (group I/R).1 hour reperfusion following ischemia 30min(group I/R 1h),2 reperfusion following ischemia 30min (group I/R 2h) and 4 reperfusion following ischemia 30 min (group I/R 4h).The contents of glutamic-pyruvic transaminase (GPT) and alkaline phosphatase (AKP),γ-glutamyl transpeptidase(γ-GT) in the serum were examined,respectively and liver tissue was observed by HE staining.The expression of iNOS in liver tissue were examined by immunohistochemical technique in each group. The changes of hepato- cellular apoptosis were measured by in situ cell apoptosis technique. Results During I/R,the remarkable liver cellular injury can be found,and the liver cellular edema,inflammatory cellular infiltration, even cellular necrosis and matched enzyme in serum increased. The contents of iNOS rose in I group (P<0.01)and reached to the peak in I/R4h group.Apoptosis exponent in group I/R was significantly higher than that in group of sham operation(P<0.01),and the exponent was increasing endlessly following the process of reperfusion injury .And there was a positive corelation between the expression of iNOS and apoptosis exponent (P<0.01,r=0.952).Conclusion Liver I/R injury leads to liver tissues injury as well as liver cellular apoptosis.The development of liver cellular apoptosis is related to the expression of iNOS.更多还原