Effect of hesperetin on cardiac fibroblast proliferarion induced by TGF-β1

HU Zhefu; TANG Qizhu; LIU Yuan; LI Jin; ZHANG Wenbin

doi:10.3969/j.issn.1671-6450.2015.04.014

Abstract：Objective To investigate the effect of hesperetin ( HES) on transforming growth factor-β1 ( TGF-β1 ) car-diacfibroblastsinducedcellproliferation,andtoexploreitspossiblemechanism.Methods 30SDratswereincluded;take the myocardial tissues to culture the fibroblasts.And then uses the TGF-β1 (10 ng/ml) to stimulate fibroblast cells, with 4 different concentrations of HES (25 μmol/L, 50 μmol/L, 75 μmol/L, 100 μmol/L) to intervene fibroblasts for 24 h, blue staining was used to detect the effect on cell viability by trypan; enzyme-linked fluorescent immunoassay testing method was used for the detection of intracellular reactive oxygen species (ROS) level;living cell counting Kit (CCK-8) was used to de-tect the proliferation of fibroblasts.Results Trypan blue staining results indicated that, HES had no significant effect on fi-broblast activity in cells, each activity values were blank control group:100%,HES 25μmol/L group:95%,HES 50μmol/L group:94%,HES 75 μmol/L group:93%,HES 100 μmol/L group:93%,enzyme mark instrument results show that, com-pared with the blank control group, TGF-β1 can increase the level of ROS in fibroblast cells ( P <0.01), when HES and TGF-β1 have effect at the same time, ROS levels decreased gradually with the increase of HES concentration, there were sta-tistical significance ( P <0.05); TGF-β1 could stimulate the proliferation of fibroblasts ( P <0.01), when HES (100μmol/L) or N-acetylcysteine (NAC) (1 mmol/L) and TGF-β1 have effect at the same time, they can inhibit fibroblast prolif-eration ( P <0.01).Conclusion Through inhibiting TGF-β1 induced oxidative stress, HES can inhibit the proliferation of cardiac fibroblasts, which suggested that it may have potential for the prevention of myocardial fibrosis.