一氧化氮合酶在实验性急性胰腺炎胰腺组织中基因表达的研究

Study of gene expression of nitric oxide synthase in the pancreatic tissues of experimental acute pancreatitis.

目的 :探讨急性胰腺炎 (AP)发病机制中与一氧化氮 (NO)的关系。方法 :采用实验性急性胰腺炎的动物模型 ,对AP形成后不同时相的胰腺组织中一氧化氮合酶 (cNOS)的基因表达进行了检测。同时检测了血清淀粉酶、红细胞超氧化物歧化酶(SOD )和病理组织。结果 :术后24小时已形成出血性、坏死性AP ,胰腺组织cNOSmRNA在术后36小时达高峰 ,随着时间的延长 ,cNOSmRNA进一步下降。结论 :在AP初期 ,NO主要由cNOS产生 ,以保护为主 ,以后cNOS下降 ,可导致AP发生不可逆损害 ,临床可通过寻找特异性诱cNOS试剂 。

Objective:To study the relationship between acute pancreatitis(AP)and nitric oxide(NO).Methods:AP was induced in rats(N=36) with the use of a closed duodenal loop technique,animals were killed at the period of 24?36?48h after induction of AP.The normal rats(N=12) were served as control.The degrees of serum amylase,erythrocytic superoxide dismutase and histopathologic alterations were investigated.At the same time the level of the subtypes of nitric oxide synthase(cNOS)mRNA in pancreatic tissues was measured by using RT-PCR with β-actin as an inner reference.Results:Hemorrhagic necrotizing AP was induced by the time of 24h after operation similar to that found in man.As compared with control group,serum amylase level was markedly at 24h(P<0.01).During AP,the cNOSmRNA was expressed,and not altered group(P<0.01),forming a peak of cNOS gene expression,then decreased at 48h.Conclusion:The expression of cNOSmRNA was mainly in the prelimimary stage of AP in order to prevent from irreversible injury.It clearly implied to us:through taking some measures to produce cNOS to ameliorated the symptom and sign of AP.