Objective To observe the effect of Modified Huangqi Chifeng Decoction (MHCD) on TGF-β₁/Smad signal pathway, and to explore its anti-renal fibrosis mechanism. Methods Adopting ser- um pharmacology method, rats were intragastrically administered with MHCD and telmisartan to prepare drug containing serum. Mouse mesangial cells were cultured in vitro, using lipopolysaccharides (LPS) as stimulating factor. The cells were divided into six groups, i.e., the normal group, the model group, the telmisartan group, high, medium and low dose MHCD groups. The cell supernatant was collected in each group after mouse mesangial cells were intervened by drug containing serum for 72 h. Contents of laminin (LN) and fibronectin (FN) were measured using ELISA. Protein expression levels of TGF-P, , p-Smad2/3, Smad7, and connective tissue growth factor (CTGF) were detected using Western blot. Results (1) Compared with the normal group, contents of LN and FN in supernatant significantly increased in the model group (P0. 01). Compared with the model group, contents of LN and FN were significantly reduced in the telmisartan group and the medium dose MHCD group (P0. 05, P0. 01). FN content in su- pernatant significantly decreased in the low dose MHCD group (P0. 01). (2) Compared with the normal group, protein expressions of TGF-β₁ , p-Smad2/3, and CTGF were significantly increased, Smad7 protein expression significantly decreased in the model group, with statistical difference (P0. 01). Compared with the model group, protein expressions of TGF-β₁ and CTGF significantly decreased in the telmisartan group and 3 MHCD groups (P0. 01 , P0. 05) ; protein expression of p-Smad23 significantly decreased in the telmisartan group, high and medium dose MHCD groups (P0.01); Smad7 protein expression were significantly increased in high and medium dose MHCD groups (P0. 05). Conclusion MHCD could inhibit increased inflammatory factors induced secretion of extracellular matrix in glomerular mesangial cells, and restrain excessive activation of TGF-β₁/Smad signal pathways, which might be one of its anti-renal fibrosis mechanisms.
