摘要
目的:前期研究表明酪酸梭菌对损伤的胃黏膜具有保护作用,但具体效应物质不明。本文通过检测酪酸梭菌的主要代谢产物氢气和丁酸对损伤胃黏膜的效应,探究黏膜保护作用的具体机制。方法:将雄性ICR小鼠通过乙醇灌胃诱导胃黏膜损伤,并以氢气和丁酸分别进行处理,观测胃组织的大体变化和组织结构损伤情况,通过RT-q PCR检测炎症因子白细胞介素12(IL-12)、Ras相关核蛋白1(RAN1)和单核细胞趋化蛋白1(MCP-1)的含量,采用免疫组化法观测Bcl-2和Bax蛋白表达量变化。结果:胃组织大体观测发现丁酸能够保护胃黏膜,而氢气不具有此作用;HE染色也提示丁酸能够显著改善乙醇造成的胃黏膜病理损伤。RT-q PCR则显示所检测炎症因子IL-12、RAN1和MCP-1的表达量较模型对照组有显著降低(P<0.01)。在丁酸组,Bax的表达量较模型组显著减低(P<0.01),而Bcl-2的含量却明显提高(P<0.01)。结论:酪酸梭菌胃黏膜保护效应的主要产物可能是丁酸而不是氢气。丁酸能够通过抑制炎症反应,下调Bax/Bcl-2表达比例,从而实现对胃黏膜的保护作用。
AIM：To observe the antiulcer effect of butyric acid and hydrogen , the main metabolites of Clos-tridium butyricum （C.butyricum）, and to explore the underlying mechanism .METHODS： The mouse model of acute gastric mucosal lesion was prepared by gavage with ethanol .The mice were randomly divided into 4 groups：normal group , model group , butyric acid group and hydrogen group .The mice in butyric acid group and hydrogen group were given buty-rate and hydrogen prior to model establishment , respectively .Macroscopic observation of the pathological changes in gastric tissues was performed to evaluate the effect of the 2 metabolites of C.butyricum.Meanwhile, the mRNA expression levels of inflammatory factors, such as IL-12, RAN1 and MCP-1, were determined by RT-qPCR.The expression levels of apopto-sis-related proteins Bcl-2 and Bax were detected by immunohistochemical staining .RESULTS：The macroscopic observa-tion found that butyrate , not hydrogen , protected gastric mucosa .HE staining also showed that butyrate significantly attenu-ated the pathological damage of the gastric mucosa induced by ethanol .Compared with model group , the mRNA levels of inflammatory factors IL-12, RAN1 and MCP-1 in butyrate group significantly decreased （P〈0.01）.In butyrate group, the protein level of Bax was obviously decreased compared with model group （P〈0.01）, while the protein level of Bcl-2 was significantly increased （ P〈0.01 ） .CONCLUSION： The gastric mucosa protective metabolite of C.butyricum may be butyric acid , not hydrogen .Butyric acid protects the gastric mucosa against ethanol-induced lesion by inhibiting the inflam- mation and reducing the expression ratio of Bax/Bcl-2.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2017年第10期1906-1911,共6页
Chinese Journal of Pathophysiology
基金
浙江省科技厅项目(No.2017C33068)
浙江省新苗人才计划(No.2017R413042)
温州市科技局项目(No.y20150009)
关键词
丁酸
氢气
急性胃黏膜损伤
炎症
细胞凋亡
Butyric acid
Hydrogen
Acute gastric mucosal lesion
Inflammation
Apoptosis
