Abstract:

AIM: To observe the effect of traditional Chinese medicine Yuxia capsule(YXC) on renal fibrosis in spontaneously hypertensive rats(SHR) and its relationship with TGF-β1/Smads signaling pathway.  METHODS: Twenty-eight 14-week-old male SHR were randomized into four groups (n=7), i.e. SHR group (0.5% CMC-Na, 5 mL/kg), YXC high dose group (0.6 g/kg), middle dose group (0.3 g/kg) and low dose group (0.15 g/kg). Another 7 wistar-kyoto( WKY) rats were selected as normal group (0.5% CMC-Na, 5 mL/kg). Animals in each group were intragastrically administrated with YXC once a day for consecutive 10 weeks. Blood pressure was measured before administration and every two weeks during administration by tail cuff method. After the last administration 24 h urine was collected and the urine micro albumin (U-mALb) levels were detected. Serum levels of beta 2-microsphere protein (β2-MG)， plasma and renal tissue angiotensin II (AngII) were measured. Changes of renal histology and collagen fibers were observed under HE and Masson staining. Expressions of TGF-β1, Smad4, Smad7 protein and Smad2/3 protein phosphorylation were detected in renal tissues by Western blot. RESULTS: Compared with model group, YXC significantly decreased the blood pressure of SHR, levels of U-mALb, β2-MG, plasma and renal tissue AngII (P<0.01 or P<0.05), and it significantly ameliorated the renal pathological tissue damage and the collagen fiber deposition. Expressions of TGF-β1, Smad4 proteins and phosphorylation of Smad2/3 protein level in YXC group were lower than those in model group, while Smad7 protein expression was higher(P<0.01).CONCLUSION: Traditional Chinese medicine YXC demonstrated protective effects against renal injury in a dose-dependent manner within a certain range in SHR, of which the potential mechanism may be related to decreasing the blood pressure, down-regulating AngII level and inhibiting the excessive activation of TGF-β1/Smads signaling pathway.

Key words: Yuxia capsule, spontaneously hypertensive rats, renal fibrosis, AngII, TGF-β1/Smads signaling pathway