Basic & Clinical Medicine ›› 2018, Vol. 38 ›› Issue (10): 1422-1427.
Objective To observe the protective effects of nitidine chloride on renal injury in diabetic nephropathy rats, and to investigate the underlying mechanisms. Methods All rats were divided into four groups: control group, diabetic nephropathy group, and diabetic nephropathy treated with nitidine chloride (20mg/kg or 40mg/kg) groups. In addition to control group, the rest of the rats were induced for diabetic nephropathy model. After the animal model was successfully established, diabetic nephropathy rats were received nitidine chloride at dose of 20mg/kg or 40mg/kg by gavage once a day, for 7 weeks. The levels of serum insulin and glucagon were determined by commercial detection kit. The pathological morphology of kidney tissues was observed by PAS staining. Cell apoptosis in glomerular was detected by TUNEL staining. The phosphorylation of Smad2 and Smad3 and the protein expression of TGF-β1 and Smad7 were analyzed by western blotting. Results After treatment with nitidine chloride, insulin level in the serum was increased, whereas the glucagon level was decreased. PAS staining showed that weak positive staining and diffuse glomerular sclerosis in low dose group. Moreover, no thickening matrix structure and renal tubular lesion could be observed in high dose group. Finally, western blotting showed that the phosphorylation of Smad2 and Smad3 and the protein expression of TGF-β1 and Smad7 in kidney tissues were significantly decreased after nitidine chloride administration.Conclusion Nitidine chloride protects against renal injury in diabetic nephropathy rats via inhibition of TGF-β/Smad signaling pathway.
TGF-β/Smad signaling pathway
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