Effects of Astragalus membranaous on the proliferation and transforming growth factorβ1 production of cardiac fibroblasts / 临床儿科杂志

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.

Effect of angiotensin II and aldosterone on the proliferation of cardiac ifbroblasts in rats / 中南大学学报(医学版)

Objective:To investigate the effect of angiotensin II (ang II), aldosterone (ald) and their receptor antagonists losartan (los) and spironolactone (spi) on the proliferation and collagen production of cardiac ifbroblasts (CFs) in rats. Methods:CFs were isolated from neonatal SD rats by collagenase II method and puriifed with differential attachment and detachment method. The 3 or 4 passages of the CFs were divided into the following groups:angiotensin II, angiotensin II+aldosterone, aldosterone, angiotensin II+losartan, and aldosterone+spironolactone. The cell viability of the CFs was assessed by Cell Counting Kit-8 (CCK-8) after the drug administration. The mRNA and protein expression levels of COL1A1, COL3A1, MMP1 and TIMP1 were detected by reverse transcription polymerase chain reaction (RT-PCR) and Western blot respectively. Results:Ang II and Ald facilitated the proliferation rate of the CFs independently compared with that in the control group (38.5%vs 28.5%;P Conclusion:Ang II and ald can promote the proliferation of CFs, and the COL1A1 and COL3A1 expression is enhanced both at mRNA and protein levels. Ang II and ald have synergistic effect when they are used together, while los and spi may restrain the effect. The mechanism is probably linked with the balance of MMPs/TIMPs.