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下丘脑室旁核对大鼠胃黏膜细胞缺血/再灌注诱导的凋亡和增殖的影响。

Effects of hypothalamic paraventricular nuclei on apoptosis and proliferation of gastric mucosal cells induced by ischemia/reperfusion in rats.

作者信息

Li Li, Zhang Yong-Mei, Qiao Wei-Li, Wang Lin, Zhang Jian-Fu

机构信息

Department of Pathophysiology, Xuzhou Medical College, Xuzhou 221002, Jiangsu Province, China.

出版信息

World J Gastroenterol. 2007 Feb 14;13(6):874-81. doi: 10.3748/wjg.v13.i6.874.

Abstract

AIM

To investigate the effects of electrical stimulation of hypothalamic paraventricular nuclei (PVN) on gastric mucosal cellular apoptosis and proliferation induced by gastric ischemia/reperfusion (I/R) injury.

METHODS

For different experimental purposes, stimulating electrode plantation or electrolytic destruction of the PVN was applied, then the animals' GI/R injury model was established by clamping the celiac artery for 30 min and allowing reperfusing the artery for 30 min, 1 h, 3 h or 6 h respectively. Then histological, immunohistochemistry methods were used to assess the gastric mucosal damage index, the gastric mucosal cellular apoptosis and proliferation at different times.

RESULTS

The electrical stimulation of PVN significantly attenuated the GI/R injury at 30 min, 1 h and 3 h after reperfusion. The electrical stimulation of PVN decreased gastric mucosal apoptosis and increased gastric mucosal proliferation. The electrolytic destruction of the PVN could eliminate the protective effects of electrical stimulation of PVN on GI/R injury. These results indicated that the PVN participated in the regulation of GI/R injury as a specific area in the brain, exerting protective effects against the GI/R injury, and the protection was associated with the inhibition of cellular apoptosis and the promotion of gastric mucosal proliferation.

CONCLUSION

Stimulating PVN significantly inhibits the gastric mucosal cellular apoptosis and promots gastric mucosal cellular proliferation. This may explain the protective mechanisms of electrical stimulation of PVN against GI/R injury.

摘要

目的

探讨电刺激下丘脑室旁核(PVN)对胃缺血/再灌注(I/R)损伤诱导的胃黏膜细胞凋亡及增殖的影响。

方法

根据不同实验目的,采用PVN刺激电极植入或电解毁损,然后通过夹闭腹腔动脉30分钟,分别再灌注30分钟、1小时、3小时或6小时建立动物胃I/R损伤模型。随后采用组织学、免疫组织化学方法评估不同时间点的胃黏膜损伤指数、胃黏膜细胞凋亡及增殖情况。

结果

PVN电刺激可显著减轻再灌注后30分钟、1小时和3小时的胃I/R损伤。PVN电刺激可减少胃黏膜凋亡并增加胃黏膜增殖。PVN电解毁损可消除PVN电刺激对胃I/R损伤的保护作用。这些结果表明,PVN作为脑内特定区域参与胃I/R损伤的调节,对胃I/R损伤发挥保护作用,且该保护作用与抑制细胞凋亡及促进胃黏膜增殖有关。

结论

刺激PVN可显著抑制胃黏膜细胞凋亡并促进胃黏膜细胞增殖。这可能解释了PVN电刺激对胃I/R损伤的保护机制。

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