Experimental study on the inhibition of Necroptosis and Epithelial-Mesenchymal Transi-tion by Yitangkang to Mitigate Diabetic Nephropathy-Induced Renal Injury
Objective This study aims to explore the effects of Yitangkang(YTK)onkidney injury indiabetic nephropathy.It further investigates the role and mechanism of YTK in epithelial-mesenchymal transition(EMT)and necroptosis-related path-ways.Methods HK-2 cells were divided into five groups:NG(normal glucose),HG(high glucose),HG+NEC-1,HG+YTK,and HG+DAPA.Animal subjects were categorized into normal control,model,positive control,and YTK high,medium,and low dose groups.Cell proliferation viability and apoptosis levels were measured using CCK-8 assay and flow cytometry,re-spectively.Renal tissue morphology and ultrastructure were observed through HE and Masson staining,and transmission electron microscopy.The expression of necroptosis and EMT-related proteins in cells and renal tissues was detected by Western blot.Re-sults After treatment with YTK,proliferation viability of HK-2 cells enhanced,and apoptosis rates were reduced(P＜0.05).Levels of necroptosis and EMT-related proteins,including RIP1,RIP3,MLKL,Vimentin,α-SMA,decreased,while E-cadherin levels increased in vitro and vivo level(P＜0.05).Conclusion YTK can alleviate kidney damage caused by diabetic ne-phropathy.Its mechanism may be related to the inhibition of necroptosis and the occurrence of EMT.
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