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GdCl_3 attenuates the glomerular sclerosis of STZ-induced diabetic rats via inhibiting TGF-β/Smads signal pathway

Jialin Li  Bing Wu  Haibo Hu  Xiansong Fang  Zhiping Liu  Suzhen Wu  
【摘要】:Background/Aims:Diabetic nephropathy(DN) is the most serious end-stage renal disease which characterized by renal glomerular sclerosis including glomerular hypertrophy,basement membrane thickening,mesangial expansion and renal fibrosis.TGF-β/Smads signal pathway plays a crucial role in the development of renal fibrosis,it is activated both in DN cell model and animal model.Gadolinium is a rare metal which has been widely used in experimental research.Methods:High glucose was used to stimulate the primary mesangial cells as DN cell model,and STZ was used to inject rats as DN animal model.Incubated mesangial cells or injected diabetic rats with GdCl_3 to evaluate the renal protective effects and its molecular mechanism of GdCl_3 by Western Blot,Co-Immunoprecipitation,tracking the location of cell membrane receptor,HE staining,PAS staining,Masson staining and immunohistochemistry.Results:Results showed that Gadolinium could repress the activation of TGF-β/Smads signal pathway induced by TGF-β1 or high glucose and then alleviated the accumulation of extracellular matrix(ECM) in mesangial cells and the kidney of type 1 diabetic rats.Further study indicated that GdCl_3 could induce the binding of CaSR and TβRⅡ and then both of these two membrane receptors translocated from cell membrane to cytoplasm,in this case,TβRⅡ on the cell membrane was decreased and then desensitized to the stimulation of its ligand TGF-β1,so that the activation of its downstream factors such as smad2 and smad3 were blocked,finally,ECM expression in mesangial cells were inhibited.Conclusions:We concluded that GdCl_3 could alleviate the accumulation of ECM in mesangial cells via antagonizing TGF-β/Smads signal pathway in diabetes mellitus.

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