Effect of Dioscin on renal tubular epithelial cells with diabetic nephropathy
Objective:To investigate the effect and mechanism of Dioscin on renal tubular epithelial cells with diabetic nephropathy.Method:Diabetic nephropathy rat model was established,and the rats were divided into control group,model group,Dioscin low-dose group,Dioscin medium-dose group,Dioscin high-dose group.Dioscin low,medium and high dose groups were given different concentrations of Dioscin(20,40,80 mg/kg)by gavage,while the control group and model group were given equal amount of saline.Normal rat renal tubular epithelial cells were collected and cultured,and divided into the blank control group,the high glucose group,the Dioscin low-dose group,the Dioscin medium-dose group,and the Dioscin high-dose group,and the Dioscin groups were given different concentrations of Dioscin(20,40,80 μmol/L);H-E staining was used to observe the pathological changes of renal tissue;RT-qPCR was used to detect the mRNA level of platelet-derived factor-BB(PDGF-BB).ELISA was used to detect the 24 h urine albumin level and the levels of tumour necrosis factor-α(TNF-α),interleukin 1β(IL-1β),reactive oxygen species(ROS),and malondialdehyde(MDA)in the epithelial cells of the renal tubule.Flow cytometry was used to detect the rate of apoptosis.PDGF-BB protein expression was detected by immunoblotting.Results:Compared with the model group,urinary albumin and renal tissue PDGF-BB mRNA levels were reduced in the Dioscin groups in a dose-dependent manner,and renal histopathological injury was improved.In the cellular experiments,PDGF-BB mRNA and protein levels,the content of TNF-α,IL-1β,MDA,ROS,and apoptosis were reduced in renal tubular epithelial cells of the Dioscin group in a dose-dependent manner,compared with that of the high glucose group.Conclusion:Dioscin can inhibit the inflammatory reaction,peroxidation damage,and apoptosis of renal tubular epithelial cells in diabetic nephropathy rats,reduce the expression of PDGF-BB,and protect renal tubular epithelial cells.
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