慢性肾小球肾炎（CGN）为临床多发难治疾病，严重威胁人类健康，经方真武汤治疗CGN有确切疗效。免疫炎症导致的足细胞损伤是CGN的核心病理基础，NLRP3炎症小体活化是足细胞重要损伤机制。课题组发现真武汤可通过抑制PI3K/AKT通路促进肾脏自噬，基于线粒体自噬在炎症小体活化及足细胞功能中的关键调节作用，我们提出“真武汤可能通过PI3K/AKT/mTOR诱导线粒体自噬，进而抑制NLRP3炎症小体活化，减少足细胞损伤治疗CGN”。本课题拟采用基因沉默、激光共聚焦、流式细胞技术、荧光定量PCR等手段，从动物及细胞模型探讨NLRP3炎症小体在CGN中的作用，研究线粒体自噬对NLRP3炎症小体活化的调控作用，明确CGN的治疗新靶点。结合真武汤对PI3K/AKT/mTOR自噬通路的干预，探讨真武汤对CGN线粒体自噬及NLRP3炎症小体活化的影响，阐明其治疗CGN的机制，为慢性肾脏疾病治疗提供科学依据。

Chronic glomerulonephritis (CGN) is a multiple and intractable disease which seriously threats human health. A classic prescription Zhen-wu-tang was confirmed efficacy on curing CGN both in clinic and experiment researches. The main pathological basis of CGN is podocyte lesion caused by immune inflammation. NLRP3 inflammasome activation may cause serious podocyte lesion. Meanwhile, it has been proved that mitophagy plays a critical role in NLRP3 inflammasome inactivation and podocyte protection. Further, our previous study found that Zhen-wu-tang could induce autophagy in kidney via PI3K/AKT pathways. Based on the above mentioned, we put forward a hypothesis that Zhen-wu-tang could induce mitophagy through suppressing PI3K/AKT/mTOR pathways, which would further inactivate NLRP3 inflammasome and reduce podocyte lesion, subsequently cure CGN. The present investigation is designed to confirm the relationship between NLRP3 inflammasome activation and podocyte lesion in CGN, analyze the regulation of mitophagy to NLRP3 inflammasome inactivation, and investigate the regulatory mechanism of Zhen-wu-tang on PI3K/AKT/mTOR pathways in CGN. All these experiments are conducted on CGN rat model and LPS-treated podocyte cell model by means of small interfering RNA, laser confocal microscopy, flow cytometry, RT-PCR. To sum up, the ultimate aim of this study is to explore the effect of Zhen-wu-tang on NLRP3 inflammasome inactivation with the modulatory function of mitophagy through PI3K/AKT/mTOR pathways, which will eventually reveal the mechanism of Zhen-wu-tang on podocyte lesion and provide a reference for the treatment of CGN.