乙酸钠通过抑制过度炎症反应保护乙醇诱导的小鼠胃黏膜损伤

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摘要目的：检测乙酸钠对乙醇诱导的胃黏膜损伤的保护作用，并探讨其内在机制。方法：小鼠随机分为正常对照组、模型组和乙酸钠组。采取乙醇诱导胃黏膜损伤模型，成模后取胃组织标本行大体观测评估疗效，采用实时荧光定量PCR技术，对炎症因子IL-1β、TNFα和MCP-1进行检测。在人正常胃黏膜细胞株GES-1上，以乙醇进行刺激，通过CCK-8检测乙醇对细胞的损伤程度。在离体培养小鼠巨噬细胞J774上，采用LPS诱导建立体外炎症反应模型，通过检测炎症因子的变化情况，评价乙酸钠对炎症反应的抑制能力。结果：与正常对照组相比，模型组乙醇诱导能明显引起胃黏膜损伤，呈现大面积的出血性损伤，而乙酸钠组明显降低乙醇诱导的胃黏膜损伤。炎症因子的检测结果发现，相较正常对照组，乙醇诱导的胃黏膜损伤造成IL-1β、TNFα和MCP-1不同程度的表达增加（P＜0.01），在乙酸钠处理后，各炎症因子的表达均明显降低（P＜
0.01）。离体培养的GES-1细胞损伤实验的结果表明，乙酸钠对乙醇引起的胃黏膜细胞GES-1损伤具有明显的保护作用。J774的细胞学实验也表明，乙酸钠显著减低IL-1β、TNFα和MCP-1的表达（P＜0.01）。结论：乙酸钠具有抗乙醇诱导的胃黏膜损伤作用，对胃黏膜细胞的保护和抑制过度的炎症反应是其重要的机制。

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	施伊露
	张佳丽
	乔莞宁
	陈洁
	苏炜
	张铮铮
	董人杰
	王方岩
	黄颖鹏

关键词 ：乙酸钠, 胃黏膜, 炎症因子, 乙醇, 小鼠

Abstract：Objective: To observe the effect of acetate sodium on the gastric mucosal lesion induced by ethanol and investigate the underlying mechanism. Methods: Mice were randomly divided into normal control group, model group and acetate sodium group. The gastric mucosal inflammation model was made by intragastric administration of ethanol. The inflammatory cytokines IL-1β, TNFα and MCP-1 were detected by real time quantitative PCR (RT-qPCR). CCK-8 was detected to evaluate the effect of acetate on the alcohol-induced injury of GES-1 which is normal cell line of human gastric mucosa. We also observed the effect of acetate sodium on the LPS-induced inflammation in the mice macrophage cell line J774 by detecting the inflammatory cytokines, IL-1β, TNFα and MCP-1. Results: Compared with normal control group, the ethanol stimulation significantly induced gastric mucosal lesion. However, acetate sodium dramatically reduced this lesion. The RT-qPCR results showed that the increased expressions of IL-1β, TNFα and MCP-1 after ethanol administration were obviously attenuated by acetate sodium (P<0.01). CCK-8 results indicated that acetate was significantly protective against the lesion induced by alcohol. The results of in vitro inflammation experiment on J774 showed that acetate sodium reduced the up-regulated expressions of IL-1β, TNFα and MCP-1 (P<0.01). Conclusion: Acetate sodium can attenuate ethanol-induced in gastric mucosal lesion. The anti-inflammation and protection against acetate in gastric mucosa play important roles in the corresponding mechanism.

Key words： acetate sodium gastric mucosa inflammatory mediators ethanol mice

收稿日期: 2018-01-29

基金资助:温州市科技计划项目（Y20150009）；浙江省科技计划项目（2017C33068）；温州医科大学仁济学院课题（wyrj20160102）；浙江省新苗人才计划项目（2017R413042）。

通讯作者: 黄颖鹏，副主任医师，Email：171121477@qq.com。

作者简介: 施伊露（1995-），女，浙江温州人，本科生。

链接本文:

https://xb.wmu.edu.cn/CN/ 或 https://xb.wmu.edu.cn/CN/Y2018/V48/I10/759

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