大鼠应激性胃黏膜损伤时细胞发生凋亡

Apoptosis in the gastric mucosa with stress induced damage

目的探讨急性胃黏膜损伤时细胞凋亡形式及作用。方法制备大鼠水浸-束缚应激(WRS)模型,计算溃疡指数(UI);TUNEL法检测胃黏膜细胞凋亡;透射电镜观察细胞形态;免疫组化法检测BCl-2/BAX蛋白的表达。结果与正常大鼠比较,WRS后2h,黏膜损伤严重(P<0.01),凋亡细胞明显增多(P<0.01),BCl-2表达明显减弱(P<0.05),BAX表达明显增加(P<0.01);WRS后24h,黏膜修复,凋亡细胞仍高于正常水平(P<0.05),BCl-2表达基本恢复正常,BAX表达仍高于正常水平(P<0.05)。透射电镜下可见WRS组发生凋亡的细胞形态各异。结论细胞凋亡是急性胃黏膜损伤过程中细胞死亡的重要形式。

Objective To investigate the mechanism of the gastric epithelial cell death with stress induced damage. Methods Water immersion-restraint stress model was developed with SD rats, Apoptotic cells were quantita- ted in gastric mucosa by terminal deoxynucleatidyl transferase mediated dUTP nick and labelling （TUNEL） techniques and electronmicroscopy while the BCl-2/BAX proteins were detected by immunohistochemical staining. Results Comparing with the control groupe, at 2 h after the WRS, the mucosa seriously damaged, the apoptotic quantities rose significantly （ P 〈 0. 01 ）, The expression of BCL-2 Protein significantly decreased （ P 〈 0. 05 ）, while BAX increased significantly （P 〈0. 01 ）, At 24 h after WRS, the apoptotic cells gradually declined but failed to returned to normal （ P 〈 0. 05 ）, the expression of BAX remained significantly higher （ P 〈 0. 05 ） but BCL-2 returned to normal level. The electronmicroscopy showed apoptotic characteristics. Conclusion The apoptosis is an important mechanism of cell death of the gastric mucosa with stress damage.