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目的 探讨生长抑素治疗小鼠急性胰腺炎对胰腺细胞凋亡及凋亡调控基因ｐ５３ 、ｂａｘ 的影响。方法 以蛙皮素诱导ＣＤ１ 小鼠急性胰腺炎模型，并应用ＴＵＮＥＬ 染色、免疫组化ＳＰ技术等检测胰腺细胞凋亡及凋亡调控基因ｐ５３ 、ｂａｘ 的蛋白表达以及生长抑素治疗后对胰腺细胞凋亡及凋亡调控基因ｐ５３ 、ｂａｘ 蛋白表达的影响。结果 苏木精伊红染色观察到胰腺组织中典型的细胞凋亡形态学特征：细胞核固缩及凋亡小体形成。ＴＵＮＥＬ结果显示蛙皮素组、正常组胰腺细胞凋亡指数显著低于生长抑素治疗组。免疫组化显示正常胰腺组织未见凋亡调控基因ｐ５３ 、ｂａｘ 的表达，生长抑素治疗组胰腺细胞ｐ５３ 染色阳性率明显高于蛙皮素组，而ｂａｘ 染色阳性率虽高于蛙皮素组，但无统计学意义。结论 生长抑素治疗急性胰腺炎的机制之一可能是诱导损伤的胰腺细胞凋亡以减轻炎症反应，该细胞凋亡机制可能与凋亡调控基因ｐ５３ 的表达有关而与ｂａｘ 的表达无关。
Objective To investigate the effect of somatostatin on pancreatic cell apoptosis and p53, bax gene expression in acute pancreatitis in mice. Methods Bone morphogenetic protein 1 was induced by bombesin and the expression of p53 and bax proteins were detected by TUNEL staining and SP immunohistochemistry. Effects of apoptosis and expression of p53 and bax protein in pancreatic. Results Hematoxylin and eosin staining showed morphological features of typical apoptotic cells in pancreatic tissues such as nuclear condensation and apoptotic body formation. TUNEL results showed that the apoptotic index in normal control group was significantly lower than that in somatostatin control group. Immunohistochemistry showed that there was no expression of p53 and bax in normal pancreas. The positive rate of p53 in pancreatic cells in somatostatin treatment group was significantly higher than that in bombesin group, while the positive rate of bax staining was higher than that in bombesin group , But not statistically significant. Conclusions One of the mechanisms of somatostatin treatment of acute pancreatitis may be to induce apoptosis of pancreatic cells in order to reduce the inflammatory reaction. The mechanism of apoptosis may be related to the expression of p53, but not the expression of bax.