Effects of Astragalus membranaous on the proliferation and transforming growth factorβ1 production of cardiac fibroblasts
10.3969/j.issn.1000-3606.2015.03.021
- VernacularTitle:黄芪对心肌成纤维细胞增殖及分泌转化生长因子-β1的影响
- Author:
Tao RUAN
;
Xuehua HE
;
Liping LIU
;
Yonghua YUAN
;
Li PAN
;
Zhenyu LIU
;
Jianhong LUO
;
Shaya HU
- Publication Type:Journal Article
- Keywords:
Astragalus membranaou;
angiotensinⅡ;
cardiac ifbroblasts;
transforming growth factor β1;
in vitro
- From:
Journal of Clinical Pediatrics
2015;(3):284-286
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo observe the effect of Astragalus membranaous on angiotensinⅡ (AngⅡ)-induced transform-ing growth factor β1 (TGF-β1) production of cardiac ifbroblasts.Methods Cardiac ifbroblasts were culturedin vitro. Cells were allocated into 3 groups: control group, Astragalus membranaous groups (50, 100, 200 mg/ml), Ang II group (10-7 mol/L) and AngⅡ/Astragalus membranaous groups (50, 100, 200 mg/ml). The proliferation of each group was tested by methyl thiazolyl tetrazolium method. TGF-β1 was measured by ELISA.Results The proliferation of cardiac ifbroblasts had signiifcant difference between each groups (F=71.84,P=0.000). The proliferation of cardiac ifbroblasts with Ang II stimulation was higher than that of cells without Ang II stimulation (P<0.05). Astragalus membranaous inhibited Ang II-induced cardiac ifbroblasts proliferation dose dependently (P<0.05). The TGF-β1 production had signiifcant difference between each groups (F=786.81,P=0.000). The TGF-β1 production in AngII/astragalus membranaous groups was lower than that in Ang II group (P<0.05). The TGF-β1 production in Ang II group was the highest, and had signiifcant difference as compared to other groups (P<0.05). Astragalus membranaous inhibited Ang II-induced TGF-β1 production dose dependently (P<0.05).Conclusions Ang II can stimulate the proliferation of cardiac ifbroblasts, and promote the TGF-β1 production. Astragalus membranaous can inhibit the proliferation of Ang II-induced cardiac ifbroblasts, and reduce the TGF-β1 production of cardiac ifbroblasts.
