To explore the mechanism of breviscapine in improving diabetic nephropathy in rats.Methods:Twenty-four Wistar rats were divided into a control group(n=6)，a model group(n=9)，and a breviscapine intervention group(n=9).Streptozocin was used to induce the type 1 diabetes model in Wistar rats.The level of glycosylated hemoglobin in the blood was detected by immunoturbidimetry.The renal injury in rats was evaluated by the albumin/creatinine ratio，superoxide dismutase(SOD)，and malondialdehyde(MDA) detected by enzyme-linked immunosorbent assay(ELISA).H&E staining and transmission electron microscopy(TEM) were used to examine the pathological changes of glomeruli in the renal cortex of rats.Renal cell apoptosis was detected using TUNEL assay.The protein expression levels of phosphorylated adenosine 5'-monophosphate-activated protein kinase(p-AMPK)，phosphorylated glycogen synthase kinase-3β(p-GSK-3β)，Bcl-2-associated X protein(BAX)，and cleaved caspase-3 were detected by Western blot.Results:Compared with the model group，the breviscapine intervention group showed reduced blood glucose level and glycosylated hemoglobin content(P<0.05)，alleviated glomerular injury and renal tissue lesions(P<0.05)，increased SOD level in the urine，reduced MDA level(P<0.05)，and elevated nuclear factor E2-related factor 2(Nrf2)/Keap1 protein ratio and heme oxygenase-1(HO-1) protein level(P<0.05).Furthermore，the breviscapine intervention group also showed up-regulated p-AMPK and phosphorylated acetyl-CoA carboxylase(ACC) protein expression in the renal cortical tissues，down-regulated protein expression levels of sterol regulatory element binding protein(SREBP-1)，SREBP-2，and adipose differentiation-related protein(ADRP)(P<0.05)，reduced apoptosis of renal tissues，and decreased protein expression levels of p-GSK-3β，BAX，and cleaved caspase-3.Conclusion:Breviscapine can reduce the renal blood glucose level，activate AMPK and Nrf2 signaling pathways to inhibit renal lipid accumulation and oxidative stress，and activate the AKT signaling pathway to inhibit apoptosis induced by hyperglycemia，thereby exerting a renal protective effect.