芝麻素对AngⅡ诱导的心肌成纤维细胞增殖和胶原分泌的影响

曹雨朦1,郑书国2,赵梦秋2,任尤楠2,涂鹏程1,李方圆1,陈雪祎1,常雪允1

(皖南医学院1.临床医学院;2.药理学教研室,安徽芜湖241002)

【摘要】目的：观察芝麻素对血管紧张素Ⅱ(AngⅡ)诱导的心肌成纤维细胞(CF)增殖及胶原分泌的影响，并探讨其可能机制。方法：应用双酶消化和差速贴壁法获得纯化的心肌成纤维细胞，采用MTT法测定芝麻素对AngⅡ诱导的成纤维细胞增殖的影响，羟脯氨酸法测定胶原含量，ELISA法测定转化生长因子β1(TGF-β1)水平，比色法测定细胞总抗氧化能力(T-AOC)及丙二醛(MDA)含量。结果：芝麻素可显著抑制AngⅡ诱导的成纤维细胞增殖和胶原分泌，抑制TGF-β1表达(P<0.05或P<0.01)，同时可提高细胞抗氧化能力，减少脂质过氧化产物MDA含量(P<0.05或P<0.01)。结论：芝麻素可明显抑制AngⅡ诱导的心肌成纤维细胞增殖和胶原合成，其机制可能与提高成纤维细胞的抗氧化能力、减少氧化损伤、下调TGF-β1蛋白表达有关。

【关键词】芝麻素；心肌成纤维细胞；血管紧张素Ⅱ；氧化应激

【文献标识码】【中图号】R 285.5A

DOI【】10.3969/j.issn.1002-0217.2015.02.002

文章编号：1002-0217(2015)02-0110-04

基金项目：皖南医学院中青年科研

收稿日期：2014-06-10

作者简介：张银昌(1983-)，男，主治医师，(电话)15178548583，(电子信箱)zhangyinchang_0216@163.com；

通讯作者王强，男，副主任医师，博士，硕士生导师，(电子信箱)879870162@qq。com，.

Effect of sesamin on collagen secretion and cardiac fibroblasts proliferation induced by angioetensin ⅡCAOYumeng,ZHENGShuguo,ZHAOMengqiu,RENYounan,TUPengcheng,LIFangyuan,CHENXuewei,CHANGXueyun

Clinical School,Wannan Medical College,Wuhu 241002,China

Abstract【】Objective：To observe the effect of sesamin on the collagen secretion and proliferation of cardiac fibroblasts(CF) induced by angiotensin Ⅱ (AngⅡ)as well as the potential mechanisms.Methods:Cardiac fibroblasts were isolated from neonatal rats with trypsin and collagenase digestion and purified by differential attachment technique.MTT assay was applied to assess the effect of sesamin on the proliferation of cardiac fibroblasts after stimulation with Ang II.Hydroxyproline method was used to determine the collagen content,enzyme linked immunosorbent assay (ELISA) for measurement of TGF-β1 level,and colorimetric method for evaluation of the cellular total antioxidant capacity(T-AOC) and malonaldehyde (MDA)level.Results:Sesamin significantly suppressed AngⅡ induced CF proliferation and collagen secretion as well as TGF-β1 expression(P<0.05 or P<0.01),whereas boosted cellular T-AOC and led to decrease of MDA level(P<0.05 or P<0.01).Conclusion:Sesamin is capable of suppressing AngⅡ induced CF proliferation and collagen synthesis.The potential mechanisms might involve boosted antioxidant capacity and down-regulation of TGF-β1 expression.

【Key words】 sesamin;cardiac fibroblasts;angiotensin Ⅱ;oxidative stress

心肌纤维化(MF)是高血压心肌重构的关键病理特征之一，也是导致心脏功能衰竭的主要原因。减少胶原沉积、抑制MF，是改善高血压性心肌重构的关键环节，也是高血压治疗的重要目标之一。持续高血压可引起肾素血管紧张素系统(RAS)激活，导致循环及心脏局部血管紧张素Ⅱ(AngⅡ)水平升高，上调转化生长因子β1(TGF-β1)的表达进而导致纤维化[1]。高血压还可诱导氧化应激，损伤机体抗氧化系统，进而促进MF进程[2]，抗氧化剂能减轻心梗所致的心肌重构[3]，提示抗氧化剂可能是防治高血压心肌重构的有效措施之一。……