| Objective:To observe the effects of Gualou Qumai Tang(GLQM)on serum lipids,adipokines and nephrin of podocyte in rat diabetic nephropathy and discuss the possible mechanism.Method:Diabetic Nephropathy model was established by SD rats with high glucose and fat diet,unilateral nephrectomy and intraperitoneal injection ofstreptozotocin(STZ)induced production.After successful modeling,the rats were randomly divided into DN model group,low dose of GLQM,medium dose of GLQM,high dose of GLQM,valsartan group,and additionally set the controlgroup.The treatments were given via gastrogavage every day starting from the 4th week of modeling,groups treated with low,medium and high dose of GLQM were given via gastrogavage to 1.4,2.8,5.6 g·kg-1,valsartan group were given via gastrogavage to 4.8×10-3 g·kg-1,the control and model group were given 2.8 g·kg-1 distilled water,once a day for 12 weeks.We observed the sign of rats,serum level of triglyceride(TG),cholesterol(CHO),high density lipoprotein(HDL)and low density lipoprotein(LDL)detected by automatic biochemical analyzer,serum level ofadiponectin(APN)andleptin(LEP)by using enzyme-linked immunosorbent assay(ELISA).Then observed pathological changes of renal tissue under light microscope,morphological changes of podocyte under electron microscope and nephrin expression in renal tissue by using Western blot method.Result:Compared with the model group,the TG,CHO,LDL of low,medium and high dose of GLQM were significantly decreased(P<0.05,P<0.01),and HDL was increased significantly(P<0.05).The LEP of medium and high dose of GLQM,valsartan group were significantly decreased(P<0.01),APN was increased significantly(P<0.01).Pathological examination showed that the pathological changes of renal tissue and podocyte in the treatment group were less than those in the model group.After the intervention of GLQM,the expressions of nephrin by Western blot were raised(P<0.05).Conclusion:GLQM can reduce renal tissue and podocyte damageand delay the development of DN by improving blood-lipid metabolism,interfering adipokine and maintaining the expressions of nephrin. |