ABSTRACT
Objective To investigate the effects of notoginseng and guiding medicinals mediated notoginseng for improving the renal inter stitial fibrosis in rats with chronic kidney-disease(CKD)by regulating TGF-β signaling pathway.Methods A total of 100 male SD rats were randomly divided into five groups:normal group(NOR,n =20),model group(CKD,n =20),radix notogin-seng group(RN,n =20),radix notoginseng plus platycodi group (RNP) and radix notoginseng plus cinnamon group (RNC,n =20).Except for the NOR group,the CKD rat model in other groups was established by adenine gavage.After modeling,the NOR group and CKD group were given the same volume of normal saline by gavage,while the group RN,RNP and RNC were given corresponding drugs by gavage,for 4 weeks.After 4 weeks,the rats in each group were sacrificed for collecting serum and detecting the renal function(serum Scr,BUN),the renal tissues were taken for conducting HE and Masson staining.Then the renal tissue pathological damage severity was observed.The expressions of FN and LN in kidney tissue were detected by immunohistochemistry and the expressions of TGF-[β,α-SMA were detected by Western blot method.Results Compared with the NOR group,the model group exhibited the renal dysfunction(P＜0.01),renal interstitial severe fibrosis manifestation and increased collagen deposition(P＜0.05),and the expression of kidney tissues α-SMA(P＜0.01),TGF-β(P＜0.01),FN and LN were significantly increased.Compared with the model group,the renal function in various treatment groups was improved,Scr(P＜0.01)and BUN(P＜0.01)were significantly decreased,the renal interstitial fibrosis degree was reduced,collagen desposition was decreased(P＜0.05),renal tissue α-SMA(P＜ 0.05),TGF-β(P＜0.05),FN and LN expression were reduced to some extent,in which the effect of RNC group was stronger than that of the RN group and RNP group.Conclusion Notoginseng and guiding medicinals mediated notoginseng can retard the progression of renal interstitial fibrosis caused by adenine in CKD rat in varying degrees,its mechanism maybe reduce the expression of TGF-β protein.