The Effect And Mechanism Of Smad7 In TGF-β/Smads Signaling Pathway During Aristolochic Acid Nephropathy Cell Model

Molecular biology methods were used to overexpress or inhibit the expression of Smad7 in normal rat kidney cells and aristolochic acid nephropathy cell models. And then detect the key factors of TGF-β/Smads signaling pathway before and after Smad7 overexpression or interfering in aristolochic acid nephropathy cell models, clarify the possible mechanisms of Smad7 in the process of aristolochic acid nephropathy cell models.we screened the best concentrations of aristolochic acid I, designed and screened the optimal small interfering RNA (siRNA) and the best transfection ratio, constructed the vector pEGFP-N3-Smad7 and find its best transfection ratio, then studied the potential treatment of Smad7 in aristolochic acid nephropathy cell models.The study increased or decreased the expression of Smad7 by pEGFP-N3-Smad7 or Smad7-siRNA in aristolochic acid nephropathy cell models, showed that when Smad7 was interfered, TGF-β/Smads signal pathway would be actived significantly, the mRNA level of Smad2/3 increased, and the protein level of actived P-Smad2/3 increased, led to the kidney disease becomes more severe; when Smad7 was overexpressed, TβRI and P-Smad2/3 decreased, TGF-β/Smads signal pathway was inhibited obviously, then weakened renal fibrosis mediated by TGF-β/Smads signal pathway.