摘要
目的:探讨羟基红花黄色素A(HSYA)抑制转化生长因子β1(TGF-β1)诱导NIH/3T3细胞活化的作用。方法:NIH/3T3细胞分8组:正常对照组、HSYA对照组、TGF-β1组、TGF-β1+0.5μmol/L HSYA组、TGF-β1+1μmol/L HSYA组、TGF-β1+2μmol/L HSYA组、TGF-1+2μmol/L SB-431542和TGF-β1+SB-431542+2μmol/L HSYA组。采用四甲基偶氮唑蓝(MTT)法检测细胞的增殖;细胞划痕实验观察细胞的迁移。结果:MTT法观察结果表明:与各时间点正常对照组相比,TGF-β1作用24,48及72小时后的OD 570nm值明显升高(均P<0.01),并且同时高于TGF-β1+HSYA各组(均P<0.05)和TGF-β1+SB-43154两组。在TGF-β1作用0,2,8,12及24小时后,与正常对照组相比,细胞迁移距离明显增加(均P<0.001),并且同时高于TGF-β1+HSYA组(均P<0.001)和SB-431542组。结论:HSYA可抑制TGF-β1诱导NIH/3T3细胞活化作用并且呈现时效关系和量效关系。
Objective： To study the inhibition of HSYA on the TGF-β1-induced activation of NIH/3T3 cell. Methods： The model of TGF-β1- induced activation of NIH /3T3 cell was used and NIH /3T3 fibroblasts were divided into 8 groups： normal group,normal HSYA group,TGF-β1 group,TGF-β1 ＋ 0. 5μmol / L HSYA group,TGF-β1 ＋ 1μmol / L HSYA group,TGF-β1 ＋ 2μmol / L HSYA group,TGF-β1 ＋ SB431542 group（ 2μmol/L）,TGF-β1 ＋ SB431542 ＋ 2μmol/L HSYA group. The proliferation of the NIH /3T3 was observed with MTT assay. The migration of the NIH /3T3 was observed with wound healing assay. Results： From the data of the same time points of MTT test it can be observed that HSYA（ 0. 5μmol / L,1μmol / L or 2μmol / L）attenuated the OD570 nm value elevation induced by TGF-β1（ TGF-β1 group vs. normal group,all P〈0. 01,TGF-β1 ＋ HSYA groups vs. TGF-β1 group,all P〈0. 05）. The cell migration distance increased after TGF-β1addition and HSYA can attenuate these changes（ TGF-β1 group vs. normal group,all P〈0. 001; TGF-β1 ＋HSYA groups vs TGF-β1 group,all P〈0. 001）. And at different time points,HSYA can inhibit TGF-β1 induced NIH /3T3 cell proliferation and migration. Conclusion： It is suggested that HSYA is active to inhibit TGF-β1-induced activation of NIH /3T3 cell
出处
《心肺血管病杂志》
CAS
2015年第5期411-414,421,共5页
Journal of Cardiovascular and Pulmonary Diseases
基金
国家自然科学基金科学基金资助项目(81270103)
北京市自然基金面上项目(7132047)
北京市中西医结合心肺血管疾病研究所课题
作者简介
通信作者：金鸣，研究员，博士生导师，研究方向：红花活血化瘀作用机理研究。E-mail：jinming_bj@163．com
