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机构地区:[1]第一军医大学南方医院肝胆血管外科,广州510515
出 处:《广东医学》2004年第2期138-140,共3页Guangdong Medical Journal
基 金:广东省科技攻关项目 (编号 :99M0 4817G)
摘 要:目的 探讨生长抑素治疗大鼠急性坏死性胰腺炎时对胰腺细胞凋亡和调控基因bax及bcl- 2的影响。方法 以牛胆酸钠诱导SD大鼠急性坏死性胰腺炎模型 ,并应用TUNEL法染色和免疫组化SABC法检测胰腺组织中基因bax及bcl- 2蛋白表达及生长抑素治疗后对胰腺细胞凋亡及凋亡调控基因bax及bcl- 2蛋白表达的影响。结果 TUNEL法染色显示生理盐水治疗组胰腺细胞凋亡指数显著低于生长抑素治疗组 ,免疫组化SABC法检测生长抑素治疗组胰腺细胞bax染色阳性率高于生理盐水治疗组 ,但无统计学意义 ;生理盐水治疗组胰腺细胞bcl- 2染色阳性率明显高于生长抑素治疗组。结论 生长抑素治疗急性坏死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胰腺炎症反应 ,细胞凋亡机制可能与生长抑素抑制bcl- 2的表达有关而与促进bax的表达无关。Objective To investigate the effects of somatostatin on apoptosis-regulated gene bax and bcl-2 in acute necrotizing pancreatitis of rats. Methods Sodium tauroglycocholate was used to induce acute necrotizing pancreatitis in rats. Apoptosis of pancreatic acinar cells was detected by TUNEL method and the expression of apoptosis-regulated gene bax and bcl-2 was determined by SABC immunohistochemical technique. Results TUNEL showed the apoptotic index of pancreatic acinar cells in saline treated group was significantly lower than that of somatostatin treated group. Immunohistochemistry showed the postive rate of bax in somatostatin treated group was higher than that of saline treated group, but there was no significant difference in the postive rate of bax betweem somatostatin treated group and saline treated group; The postive rate of bcl-2 in saline treated group was significantly higher than that of somatostatin treated group.Conclusion Induction of apoptosis in injuried pancreatic acinar cells might be one of mechanisms of somatostatin in treating acute necrotizing pancreatitis in rat, and the mechanisms of apoptosis might be associated with the down-regulation of bcl-2, but has no association with the up-regulation of bax.
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