双氯灭痛胶浆对重症急性胰腺炎大鼠的治疗作用机制

The Effects and Mechanism of Diclofenac Sodium on Severe Acute Pancreatitis in Rats

目的:研究双氯灭痛胶浆对大鼠重症急性胰腺炎(SAP)的治疗作用及机制探讨。方法:将大鼠随机分成双氯灭痛胶浆治疗组(Ds)、重症急性胰腺炎组(SAP)和正常对照组(N),术后分别于12、24和36h处死,观察血清淀粉酶、SOD、CAT、NO、丙二醛(MDA)、核因子κB(NF-κB)、及胰腺大体病理及光镜下病理变化。结果:治疗组的淀粉酶、NF-κB、NO、MDA、胰腺组织的Hughes评分均明显降低、SOD、CAT、明显升高(P<0.05)。结论:双氯灭痛胶浆对大鼠SAP有治疗作用,其作用机制可能与抑制NF-κB等前致炎物质的释放,清除自由基和抗脂质过氧化反应,抑制胰腺组织中的中性粒细胞的浸润及其活化程度有关。

Objective： To study the effects and mechanism of diclofenac sodium on severe acute pancreatitis （SAP） in rats. Methotis： Fifty-six healthy male SPF rats were randomly divided into diclofenac sodium group （Ds）, SAP group and control group. Each of the former two groups was subdivided into three subgroups. Eight normal rats were used as the control group. At 12th, 24th and 36th hours after induction of SAP, eight rats in each group were respectively sacrificed. The blood samples were collected for measurement of serum amylase, SOD, CAT, NO, MDA, NF-κB. The pancreas was taken for measurement of pathologic observation. Results： The levels of amylase,NO, MDA, NF-κB and pathologic scoring of pancreas in all treatment groups were obviously lower than those of SAP group （P〈0.05）. The levels of SOD, CAT in all treatment groups were obviously higher than those of SAP group （P〈0.05）. Conclusions： Diclofenac sodium has obviously effects on severe acute pancreatitis in rats; the effects of the early is more effective than that of the late. The mechanism of diclofenac sodium is possibly associated with inhabiting the release of pre-mediator such as NF-κB and removing flee radicle anti-lipid peroxidation and inhabiting the activity of neutronphil in the pancreas.