急性胰腺炎大鼠肾上腺损伤中bax与bcl-2表达的研究

目的 观察急性胰腺炎(AP)大鼠肾上腺损伤时细胞凋亡及调控基因bcl-2和bax蛋白的表达及作用.方法 采用牛磺胆酸钠逆行胰胆管注射法建立AP模型.术后3、6、12 h检测血皮质酮水平,观察肾上腺病理,TUNEL检测细胞凋亡,免疫组织化学检测bcl-2和bax蛋白表达.结果 与SO组比较,AP3 h组血清皮质酮显著增高,随后逐渐降低(P＜0.05).随病程延长,肾上腺细胞凋亡指数增高,bax蛋白表达增强,bax/bcl-2比值亦逐渐升高(P值均＜0.05),并与凋亡指数(AI)呈正相关(r =0.759,P＜0.05).结论 bax和bcl-2可能参与了AP肾上腺损伤的发病过程.通过激活bcl-2和抑制bax的蛋白表达,减少细胞凋亡发生从而保护肾上腺结构和功能,可能为今后AP及相关肾上腺损伤的药物及基因治疗提供依据和新思路.

Expression of apoptosis-regulated genes bax and bcl-2 in pancreatitis-associated adrenal injury in rats with acute pancreatitis

Objective To investigate apoptosis and expression of apoptosis-regulated genes bcl-2 and bax protein in adrenal injury in acute pancreatitis (AP) rats.Methods AP model was induced by retrograde injection of 5％ sodium taurocholate into the bilipancreatic duct.At 3,6,and 12 h after operation,pathological changes of the adrenal were observed under light and electron microscopes,apoptosis of the adrenal cells was determined by TUNEL method,and protein expression of bcl-2 and bax was detected by immunohistochemical staining.Results Serum corticosterone level at 3 h after AP was significantly higher than in SO group,then gradually decreased ( P ＜ 0.05 ).With the duration extension of AP,apoptosis index of adrenal cells and protein expression of bax were significantly elevated ( P ＜ 0.05 ),the ratio of bax to bcl-2 was increased gradually and positively correlated with apoptosis index (r =0.759,P ＜ 0.05 ).Conclusion bcl-2 and bax may be involved in the pathogenesis of adrenal injury in AP rats.Activation of bcl2 and inhibition of bax protein expression may enable to reduce cell apoptosis,protect the structure and function of the adrenal gland,which may provide a basis for drug and gene therapy of pancreatitis and associated adrenal injury.