摘要
目的研究电刺激大鼠室旁核(PVN)对胃缺血-再灌注(GI-R)损伤的保护作用及细胞机制。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、1 h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。
Objective rio observe the effects of electrical stimulation of paraventricular nucleus （PVN） on gastric mueosal cellular apoptosis, proliferation, and expression of BCL-2, BAX induced by gastric ischemia-reperfusion （GI-R） and the potential 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 so inhibited gastric mucosal cellular apoptosis and promoted proliferation.
出处
《基础医学与临床》
CSCD
北大核心
2007年第3期238-242,共5页
Basic and Clinical Medicine
基金
国家自然科学基金(30370533
30570671)
关键词
室旁核
胃缺血-再灌注
细胞凋亡
BCL-2
BAX
paraventricular nucleus （PVN）
gastric ischemia-reperfusion （GI-R）
cellular apoptosis
BCL-2
BAX
