Key Laboratory of Animal Resistance Biology of Shandong Province, School of Life Science, Shandong Normal University, Jinan, 250014, China.
Central Laboratory, Jinan Central Hospital Affiliated to Shandong University, Jinan, 250013, China.
Sci Rep. 2018 Jul 5;8(1):10170. doi: 10.1038/s41598-018-28456-0.
Previous studies showed that restraint water-immersion stress (RWIS) increases the expression of Fos protein in the ventromedial hypothalamic nucleus (VMH), indicating the VMH involving in the stress-induced gastric mucosal injury (SGMI). The present study was designed to investigate its possible neuro-regulatory mechanisms in rats receiving either VMH lesions or sham surgery. The model for SGMI was developed by restraint and water (21 ± 1 °C) immersion for 2 h. Gastric mucosal injury index, gastric motility, gastric acid secretion and Fos expression in the hypothalamus and brainstem were examined on the 15th postoperative day in RWIS rats. Gastric mucosal injury in VMH-lesioned rats was obviously aggravated compared to the control. Gastric acidity under RWIS was obviously higher in VMH-lesioned rats than that in sham rats. Meantime, the VMH-lesioned rats exhibited marked increases in the amplitude of gastric motility in the VMH lesions group after RWIS. In VMH-lesioned rats, Fos expression significantly increased in the dorsal motor nucleus of the vagus (DMV), the nucleus of the solitary tract (NTS), the area postrema (AP), the paraventricular nucleus (PVN) and the supraoptic nucleus (SON) in response to RWIS. These results indicate that VMH lesions can aggravate the stress-induced gastric mucosal injury through the VMH-dorsal vagal complex (DVC)-vagal nerve pathway.
先前的研究表明，束缚浸水应激（RWIS）会增加腹内侧下丘脑核（VMH）中 Fos 蛋白的表达，表明 VMH 参与应激诱导的胃黏膜损伤（SGMI）。本研究旨在探讨 VMH 损伤或假手术大鼠接受 RWIS 后的可能神经调节机制。通过 2 小时的束缚和水（21±1°C）浸泡来建立 SGMI 模型。在 RWIS 大鼠的第 15 天术后，检查胃黏膜损伤指数、胃动力、胃酸分泌和下丘脑及脑干中的 Fos 表达。与对照组相比，VMH 损伤大鼠的胃黏膜损伤明显加重。在 RWIS 下，VMH 损伤大鼠的胃酸明显高于假手术大鼠。同时，VMH 损伤大鼠在 RWIS 后 VMH 损伤组的胃动力振幅明显增加。在 VMH 损伤大鼠中，RWIS 会引起背侧迷走神经核（DMV）、孤束核（NTS）、最后区（AP）、室旁核（PVN）和视上核（SON）中 Fos 表达显著增加。这些结果表明，VMH 损伤可以通过 VMH-背侧迷走神经复合体（DVC）-迷走神经通路加重应激诱导的胃黏膜损伤。
