[Effects of Chinese herbal medicine Xuefu Zhuyu Decoction on angiotensin II-induced proliferation and extracellular matrix synthesis of rat cardiac fibroblasts].

OBJECTIVE

To investigate the effects of Xuefu Zhuyu Decoction, a compound Chinese herbal medicine, on the proliferation and extracellular matrix synthesis of cardiac fibroblasts (CFs) from neonatal rats induced by angiotensin II, and to explore the mechanism of Xuefu Zhuyu Decoction in improving myocardial fibrosis.

METHODS

CFs derived from neonatal rats were cultured with enzymatic dissociation to establish a cell model of cardiac fibrosis induced by angiotensin II in vitro. CFs were divided into 6 groups, including blank control group, angiotensin II group, valsartan-medicated serum group, and 5%, 10% and 15% Xuefu Zhuyu decoction-medicated serum group. CFs in the blank control group were incubated with normal rat serum; CFs in the other groups were stimulated with angiotensin II at a dose of 10-6 mol/L, and then incubated with normal rat serum and 5%, 10% and 15% Xuefu Zhuyu decoction-medicated serum for 24 h, respectively. Methyl thiazolyl tetrazolium assay was employed to measure CF proliferation, and collagen synthesis was detected by analysis of the hydroxyproline in CFs. Radioimmunoassay was used to measure concentrations of procollagen III and hyaluronic acid. Enzyme-linked immunosorbent assay was used to measure fibronectin expression.

RESULTS

Compared with the blank control group, angiotensin II induced cardiac fibroblast proliferation, stimulated DNA and collagen syntheses (P<0.01), and increased fibronectin, hyaluronic acid and procollagen III concentrations (P<0.01). Xuefu Zhuyu decoction-medicated serum inhibited CF proliferation and DNA and collagen syntheses (P<0.05), and decreased the concentrations of fibroectin, hyaluronic acid and procollagen III (P<0.01).

CONCLUSION

Angiotensin II can induce cardiac fibrosis, stimulate cardiac fibroblast proliferation and extracellular matrix synthesis, while Xuefu Zhuyu Decoction can prevent cardiac fibrosis, the mechanism of which may be related to inhibiting CF proliferation and extracellular matrix synthesis.