Mechanism of Yitangkang(益糖康)Enhancing Podocyte Autophagy in Improving Diabetic Kidney Disease
Objective To observe the effect of Yitangkang(益糖康,YTK)on podocyte autophagy in diabetic kidney disease(DKD)rats and explore the mechanism of YTK in improving DKD.Methods A total of 96 8-week-old healthy Wistar rats were randomly divided into model control group,YTK high-dose group(40 g·kg-1),YTK middle-dose group(20 g·kg-1),YTK low-dose group(10 g·kg-1),and western medicine control group(Losartan Tablets,20 mg·kg-1).The DKD model was established by high-fat diet combined with single intraperitoneal injection of streptozotocin.Eighty-six DKD rats with success-ful model establishment were given drug intervention for 8 weeks.The levels of fasting blood glucose(FPG)was measured by a rapid blood glucose meter.Serum urea nitrogen(BUN),serum albumin(ALB),serum creatinine(Scr),serum uric acid(UA),serum total protein(TP),triglyceride(TG),total cholesterol(CHO),low density lipoprotein cholesterol(LDL-C)and high den-sity lipoprotein cholesterol(HDL-C)were measured by manual method.HE staining was used to observe the pathological mor-phology of the kidney tissue.The expressions of autophagy-related proteins(LC3-Ⅰ,LC3-Ⅱ,p62,ATG5,Beclin1)in podo-cytes were detected by Western blotting.Results Compared with those of the blank control group,the kidney tissue of the model group showed irregular cell arrangement,structural disorder and inflammatory cell aggregation.The levels of FBG,BUN,TG,CHO,LDL-C,Scr,UA and TP were significantly increased,and the levels of ALB and HDL-C were significantly decreased(P＜0.01).The expressions of LC3-Ⅰ,p62 and Beclin1 protein in renal tissue were increased,and the expressions of LC3-Ⅱ and ATG5 protein were decreased(P＜0.01).Compared with those of the model control group,the renal pathological damage of each YTK group and the western medicine control group was significantly alleviated,and the inflammatory infiltration was sig-nificantly reduced.The levels of FBG,BUN,TG,CHO,LDL-C,Scr,UA and TP were significantly decreased,and the levels of ALB and HDL-C were significantly increased(P＜0.01).The expressions of LC3-Ⅰ,p62 and Beclin1 protein in renal tissue were decreased,and the expressions of LC3-Ⅱ and ATG5 protein were increased(P＜0.01).Conclusion YTK can effectively improve renal injury in DKD rats,which may be through down-regulating the expressions of LC3-Ⅰ,p62 and Beclin1 protein and increasing the expressions of LC3-11 and ATG5 protein to regulate the level of DKD autophagy to protect the kidney.
diabetic kidney diseaseChinese medicine compound Yitangkang(益糖康)podocytesautophagymechanism research
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NSTL
万方数据
