基础医学与临床 ›› 2009, Vol. 29 ›› Issue (3): 234-237.

• 研究论文 • 上一篇    下一篇

Akt参与室旁核内注射微量催产素减轻大鼠胃缺血-再灌注损伤

张咏梅 张文文 张建福   

  1. 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:2008-04-30 修回日期:2008-06-26 出版日期:2009-03-25 发布日期:2009-03-25
  • 通讯作者: 张建福

Protective effect of Akt on gastric ischemia-reperfusion injury by microinjection of oxytocin into the paraventricular nucleus in rats

Yong-mei ZHANG, Wen-wen ZHANG, Jian-fu ZHANG   

  1. Department of Physiology, Xuzhou Medical College Department of Physiology, Xuzhou Medical College
  • Received:2008-04-30 Revised:2008-06-26 Online:2009-03-25 Published:2009-03-25
  • Contact: Jian-fu ZHANG

摘要: 目的 研究PVN内注射微量催产素(OT)对大鼠胃缺血再灌注(GI-R)损伤的影响及其局部的分子机制。方法 用夹闭大鼠腹腔动脉30 min,再灌注1 h的GI-R损伤模型,于单侧PVN内注射微量OT。计数胃黏膜损伤指数后,用免疫组化及免疫印迹观察胃黏膜细胞p-Akt和caspase-3蛋白表达。结果 PVN内注射微量OT(24、120、600和3000 ng)呈剂量依赖性减轻GI-R损伤,并明显增加胃黏膜细胞的Akt表达和减少caspase-3的表达。侧脑室给予OT特异性拮抗剂atosiban后取消OT对大鼠GI-R损伤的影响。结论 PVN微量注射OT后通过增加胃黏膜细胞Akt表达,抑制caspase-3的表达,减轻GI-R损伤。

关键词: 胃缺血-再灌注, 室旁核, 催产素, Akt

Abstract: Objective To observe the effect of microinjection of oxytocin (OT) into paraventricular nucleus (PVN) on gastric ischemia-reperfusion (GI-R) injury and its local molecular mechanism. Methods GI-R injury was induced in rats by clamping the celiac artery for30 min and then reperfusing for 1 h. A cannula was inserted into the unilateral PVN for microinjection of OT. The gastric mucosal injury index was counted grossly. The expressions of Akt and caspase-3 in rat gastric mucosa were examined by Western blot and by immunohistochemistry. Results Microinjection of OT into PVN dose-dependently attenuated gastric mucosal injury subjected to GI-R. Microinjection OT into PVN significantly increased the expression of Akt protein and decreased the level of caspase-3 in gastric mucosal following GI-R. The effects of OT were prevented by pretreatment with OT receptor antagonist atosiban into the lateral cerebral ventricle. Conclusion Microinjection of OT into PVN significantly protected against GI-R injury. These central effects of OT are mediated by its receptors. The local mechanisms were mediated by increasing Akt expression, which in turn leads to inhibit caspase-3 expression.

Key words: gastric ischemia-reperfusion (GI-R), paraventricular nucleus (PVN), oxytocin (OT), Akt

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