岭南湿热证中肠道组织自噬、线粒体DNA含量和MAVS通路介导炎症的研究

Autophagy,mtDNA Quantity And Inflammation Activated by MAVS in Intestine Tissue of Mice with Lingnan Dampness-Heat Syndrome

目的:研究岭南湿热证模型小鼠肠道组织自噬,及肠道菌群在其中的作用。方法:将SPF小鼠饲养在模拟湿热环境的人工气候箱中,诱导出类似于人的湿热证表现;并设置与多种抗生素联用的"伪无菌"组,通过PCR,Western Blot等分子生物学技术检测各组小鼠肠组织的线粒体DNA含量及MAVS、炎症小体相关通路的蛋白表达情况。结果:造模后小鼠出现类似于湿热证的改变。且各组线粒体DNA均减少,P62/SQSTM1升高、而LC3Ⅱ总量略降低,MAVS、ASC、pro-Caspase 1各组间无明显区别,pro-IL-1β在HTH组有显著性差异(P<0.05)。结论:湿热环境可能通过抑制自噬、导致mtDNA减少;肠道菌群或许对此进程有一定程度的保护作用。

Objective:To investigate inflammationand autophagy in intestine tissue of mice with Lingnan dampness-heat syndrome and the role of gut microbes play in this process.Method:SPF and pseudo-germ free mice were maintained in climate chamber for environmental controlled,leading to symptoms similar to dampness-heat syndrome.The mtDNA quantity,MAVS and inflammasome were detected by molecular biology technology such as PCRand Western Blot.Results:Dampness-heat syndrome of mice were manifested.The mtDNA quantity was down-regulated in both SPF and pseudo-germ free mice.P62/SQSTM1 increased while LC3Ⅱdecreased.There was no significant difference in MAVS,ASCor pro-Caspase 1,but pro-IL-1βshowed significant difference in high temperature and humidity group(HTH)(P<0.05).Conclusion:High temperature and humidity may inhibit autophagy and down-regulate mtDNA,while gut microbes probably play a protective role in this process.