Abstract: Objective　To investigate the role and mechanism of plumbagin in IgA nephropathy. Methods　First, the IgA nephropathy model was constructed according to the modified BSA+LPS+CCl4 method of Ying et al. Then, the rats in the administration group were intraperitoneally injected with 10 mg/kg, 20 mg/kg or 50 mg/kg of plumbagin per day. The normal group and the model group were intraperitoneally injected with the same amount of normal saline per day, after 8 weeks later, 24 h urine protein, serum creatinine, and blood urea were detected by a fully automatic chemical analyzer, and the ROS content was detected by flow, and the SOD activity and MDA content were detected. Pathological damage was observed by HE staining, TNF-a, IL-18, IL-1β were detected by Elisa, and NLRP3, ASC, caspase-1 p20, P13K, protein expression of AKT and NF-kB were detected by Western blotting.　Results　Compared with the model group, the proteinuria, serum creatinine and urea nitrogen levels of the administration group significantly reduced, ROS levels significantly decreased, SOD  levels increased, MDA, IL-1b, IL-18 and TNF-a levels were significantly increased. Protein expression of NLRP3, ASC, caspase-1 p20, P13K, AKT and NF-kB was significantly down-regulated, with the increasing of dose, the effect was more pronounced. Conclusions　Plumbagin mainly reduces IgA nephropathy by reducing urinary protein, serum creatinine and blood urea, reducing pathological damage, inhibiting oxidative stress, inflammatory response and activation of NLRP3 / P13K / AKT / NF-kB pathway.

Key words:  , Plumbagin, 　IgA nephropathy, 　ROS, 　NLRP3