摘要
目的探讨rhCD40L及阿司匹林对人I型胶原α2(I)链启动子活性的作用。方法体外培养人血管平滑肌细胞(VSMCs),人Ⅰ型胶原α2(Ⅰ)链基因启动子重组质粒pCOLH22.4和pCOLH21.6扩增和酶切鉴定后,通过脂质体(Lipofectamin)转染VSMCs,rhCD40L刺激转染后细胞,ELISA检测CAT目的基因表达以及阿司匹林(100μmol/L)的影响。结果rhCD40L使CAT目的基因表达下降;阿司匹林可以增加CAT目的基因表达,并逆转rh-CD40L诱导的CAT目的基因表达下降(P<0.05)。结论阿司匹林上调人I型胶原启动子活性表达,并且逆转rh-CD40L对人I型胶原启动子活性的下调作用,可能是其抗动脉粥样硬化和稳定斑块的机制之一。
AIM To evaluate the effect of aspirin on humanα2 （ I ） collagen promoter induced by rhCIMOL. METHODS After amplification and identification, pCOLH22.4 and pCOLH2 I. 6, a plasmid containing PCAT3-Enhaneer, were transfeeted into human VSMCs using Lipofectamin transfection reaarget gene and protein were measured by CAT ELISA kit. The effects of aspirin on CAT activity were evaluated after transfection. RESULTS After transfection, the activity of CAT reporter gene was assessed by ELISA method. Compared with those in the control group, the CAT activities were inhibited by rhCIMOL. Aspirin reversed the CAT activities inhibited by rhCIMOL. CONCLUSION Aspirin up-regulates the expression of humanα2 （ I ） collagen promoter and reverses promoter activities inhibited by rhCD40L. This may be one of the mechanism of aspirin in improving plaque stability.
出处
《心脏杂志》
CAS
2007年第5期543-546,共4页
Chinese Heart Journal
基金
国家重点基础研究发展规划项目资助(No.2005CB523309)
