基础医学与临床 ›› 2007, Vol. 27 ›› Issue (3): 238-242.

• 研究论文 • 上一篇    下一篇

电刺激室旁核减轻大鼠胃缺血再灌注损伤的胃黏膜细胞变化

李俐 张咏梅 张建福 乔伟丽   

  1. 徐州医学院病理生理学教研室 徐州医学院生理学教研室 徐州医学院生理学教研室
  • 收稿日期:2006-06-29 修回日期:2006-09-22 出版日期:2007-03-25 发布日期:2007-03-25
  • 通讯作者: 李俐

The effects of electical stimulation of paravrntricular nucleus on gastric mucosal cells in relieved gastric ischemia-reperfusion injury of rats

  

  • Received:2006-06-29 Revised:2006-09-22 Online:2007-03-25 Published:2007-03-25

摘要: 目的 研究电刺激大鼠室旁核(PVN)对胃缺血-再灌注(GI-R)损伤的保护作用极细胞机制。方法 电刺激大鼠PVN后,制备GI-R模型;用免疫组化方法检测胃黏膜细胞的凋亡和增殖以及凋亡相关基因BCL-2、BAX的表达。结果 与单纯GI-R组相比, 电刺激PVN能明显减少GI-R后30 min、1h和3 h胃黏膜细胞的凋亡,并能加快胃黏膜细胞的增殖;同时可以明显增加抗凋亡因子BCL- 2的蛋白表达,降低促凋亡因子BAX的蛋白表达。结论 电刺激大鼠PVN对GI-R损伤的保护作用可能是通过上调抗凋亡因子BCL-2、下调促凋亡因子BAX的蛋白表达,从而促进了胃黏膜细胞增殖、抑制其凋亡来实现的。

Abstract: Objective To observe the effects of electrical stimulation of paraventricular nucleus (PVN) on gastric mucosal cellular apoptosis,proliferation,and expression of BCL-2,BAX induced by gastric ischemia-reperfusion (GI-R), investigate the cellular mechanisms of protection of PVN on GI-R injury . Methods After electrical stimulation of PVN, the experimental model of GI-R were established by clamping the celiac artery for 30 min and then reperfusing the artery for 30 min,1 h,3 h,or 6 h respectively. We used immunohistochemistry to detect the gastric mucosal cells apoptosis, proliferation and the expression of BCL-2,BAX. Results Compared with GI-R group,the electrical stimulation of PVN markedly decreased gastric mucosal cellular apoptosis,increased the proliferation,and promoted the protein expression of BCL-2,but markedly inhibited the protein expression of BAX at 30 min,1 h, 3 h after reperfusion respectively. Conclusion The protective effect of PVN on GI-R injury is associated with up-regulation of expression of BCL-2 and down-regulation expression of BAX,and then inhibiting gastric mucosal cellular apoptosis and promoting proliferation induced by GI-R injury.