Objective：To observe the effect of astragaloside IV on PERK pathway in rats with passive Heymann nephritis.Methods：The rat model of passive Heymann nephritis was established by tail intravenous injection of anti-Fx1A serum.Forty SD rats were randomly divided into the normal control group，the model group，the low-dose astragaloside IV group，the high-dose astragaloside IV group and the benazepril group.After the success of model establishment，each treatment group received intragastric administration for 4 weeks.Detected 24-h urinary protein quantification periodically.After 4 weeks，sacrificed all the rats，collected blood to detect serum albumin，observed the renal pathological changes by PASM，detected the expression of phosphorylated protein kinase R-like ER kinase(p-PERK)and phosphorylated eukaryotic translation initiation factor 2α(p-eIF2α)in renal tissues by immunehistochemistry，and detected the expression of glucose-regulated protein 78(GRP78)in renal tissues by Western blot.Results：24-h urinary protein quantification of rats in the model group was significantly higher than that in the normal control group(P ＜ 0.05)，and the urine protein was gradually increased as time went by，which reached its peak after 4 weeks.After administration for 4 weeks，comparing with the normal control group，the expression of p-PERK，p-eIF2α and GRP78 in the renal tissues of rats in the model group was evidently higher，serum albumin was decreased evidently，differences being significant(P ＜ 0.05).Comparing with the model group，24-h urinary protein quantification of rats in the high-dose astragaloside IV group and the benazepril group were significantly decreased，the expression of p-PERK，p-eIF2α and GRP78 in the renal tissues was significantly decreased，and serum albumin was significantly increased，differences being significant(P＜ 0.05).Conclusion：Astragaloside IV may relieve the renal damage resulting from passive Heymann nephritison by inhibiting PERK pathway in endoplasmic reticulum stress(ERS).