基于FoxO信号通路探讨HP相关性胃炎脾胃湿热证胃黏膜细胞凋亡的机制  

Apoptosis Mechanism on Gastric Mucosa Cells of HP Associated Gastritis of Spleen-Stomach Dampness-Heat Based on FoxO Signal Pathway

作　　者：周义方 喻斌[2] 徐寅[2] 曾蓉 陈末 ZHOU Yifang;YU Bin;XU Yin;ZENG Rong;CHEN Mo(Hunan University of Chinese Medicine,Changsha 410208,China;The First Affiliated Hospital of Hunan University of Chinese Medicine,Changsha 410208,China)

机构地区：[1]湖南中医药大学,湖南长沙410208 [2]湖南中医药大学第一附属医院,湖南长沙410208

出　　处：《中医药学报》2020年第8期12-18,共7页Acta Chinese Medicine and Pharmacology

基　　金：湖南省教育厅科学研究项目(17A158)。

摘　　要：目的:采用复合病因造模法建立HAG脾胃湿热证小鼠模型,并阐明HAG脾胃湿热证模型胃黏膜细胞损伤与FoxO信号通路调控细胞凋亡的关系。方法:选取60只SPF级BALB/c小鼠,随机分为5组,采用复合病因造模法(肥甘食物+湿热环境+幽门螺杆菌),建立HAG脾胃湿热证小鼠模型。指标分析包括:胃黏膜组织病理形态及炎症程度观察;胃黏膜细胞凋亡评价;FoxO信号通路相关物质的检测(PTEN、PI3K、Akt、FoxO)。结果:正常对照组胃黏膜无明显炎症反应,模型组胃黏膜炎症呈不同程度的改变,其中以复合病因组炎症反应最明显,炎症程度最重。模型组胃黏膜细胞凋亡的阳性率较高,其中以复合病因组阳性率最高。各模型组PTEN、FoxO3a蛋白表达及基因含量水平较正常对照组高,PI3K、Akt蛋白表达及基因含量水平较正常对照组低,以复合病因组变化最为显著。结论:HAG脾胃湿热证小鼠模型胃黏膜细胞凋亡率升高,其细胞凋亡的机制与PTEN/PI3K/Akt/FoxO信号通路有关,通过激活其通路来对细胞凋亡进行调控。Objective: To establish models of HP associated gastritis(HAG) of Spleen-Stomach dampness-heat, and to clarify the relationship between gastric mucosal injury and FoxO signal pathway that regulating apoptosis. Methods: 60 BALB/c mice were randomly divided into five groups, i.e. the normal control group, the internal-dampness HP group, the external-dampness group, the simple HP group and the complex pathogenesis group. The models of HAG were established by using the complex pathogenesis(fat and sweet diet+hygrothermal environment+HP). Indicator analysis including pathological morphology and degree of inflammation of gastric mucosa tissue, apoptosis of gastric mucosa cells, and substances detection related to FoxO signal pathway. Results: There was no obvious inflammatory reaction of gastric mucosa in the normal control group;gastric mucosal inflammations could be seen in the model groups with different degrees;the inflammations were most obvious in the complex pathogenesis group. After modeling, apoptotic rate of gastric mucosa cells was increased, and the rate was increased most significantly in the complex pathogenesis group. The expression levels of PTEN and FoxO3 a were higher and the expression levels of PI3 K and Akt were lower in the model groups than those in the normal control group;the most significant changes could be seen in the complex pathogenesis group. Conclusion: The apoptotic rate in HAG model of damp-heat of Spleen and Stomach is increased, and the apoptotic negulating mechanism is related to activating PTEN/PI3 K/Akt/FoxO signal pathway.

关 键 词：复合病因 HP相关性胃炎 脾胃湿热 FoxO信号通路 细胞凋亡 

分 类 号：R285.5[医药卫生—中药学]