摘要
目的和方法 :利用组织块贴壁法进行大鼠VSMC培养 ,胰蛋白酶分散细胞法传代 ,实验采用第 4～ 6代细胞。采用氚 胸腺嘧啶核苷 ([3 H] TdR)掺入和细胞计数来作为VSMC增殖的指标 ,以RT PCR的方法检测ETAR的表达 ,观察 17β 雌二醇 (E2 )对内皮素 1(endothelin l,ET 1)介导的血管平滑肌细胞 (VSMC)增殖反应以及对内皮素A型受体(ETAR)表达的影响。结果 ::ETAR特异性拮抗剂BQ12 3能完全阻断ET 1介导的VSMC增殖反应 ;E2 可明显抑制ET 1促进VSMC增殖的作用。RT PCR结果显示E2 能抑制ETAR的表达 ,12h时抑制作用最为明显 ;E2 受体阻断剂Tamoxifen亦能部分抑制ET 1对VSMC的增殖及ETAR的mRNA的表达。结论 :ET 1促进VSMC增殖作用主要通过ETAR介导的 ,雌激素可通过抑制ETARmRNA表达来发挥对ET
Aim and Methods: To determine the effect of 17 β estradiol on proliferation of cultured vascular smooth muscle cells (VSMC) and expression of ET A receptor mRNA stimulated by endothelin 1 (ET 1). The experimental models of proliferation in cultured rat aortic smooth muscle cells induced by ET 1 was established. The 3 H thymidine ( TdR) incorporation, cell counts and reverse transcription polymerase chain reaction (RT PCR) were used in this study. Results: BQ123, the selective ET A receptor antagonist, inhibited the increase of TdR incorporation and cell number in response to ET 1 of VSMC.17 β estradiol may reverse the incrsase of TdR incorporation and cell number stimulated by ET 1. 17 β estradiol downregulated of ET A receptor mRNA expression, with the maximum at 12 hours, which was partially proventd by tamoxifen, an estrogen receptor antngonist. Conclusion: The proliferation of VSMC stimulated by ET 1 was mainly through ET A receptor. 17 β estradiol inhibited the proliferation of VSMC stimu1ated by ET 1, which might be through downregulation of ET A receptor.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2001年第3期251-254,共4页
Chinese Journal of Applied Physiology
基金
广东省科委重点科技基金资助项目 (99M0 480 8G)
