摘要
采用氚-胸腺嘧啶核苷(~3H-TdR)参入法,电镜,免疫组化,原位杂交法,观察了卡托普利(Cap)对实验性高血压大鼠血管平滑肌细胞(VSMC)增殖的作用及对热应激蛋白70 kd(HSP70)及其mRNA和抑癌基因P53表达的影响。结果发现:Cap在降低血压同时,能减少VSMC的线粒体、粗面内质网和~3H-TdR参入量(均为P【0.01),并能逆转VSMC增殖时HSP70及其mRNA表达增强(均P【0.01),P53抑癌基因mRNA表达减弱(P【0.05)。结果表明:Cap能抑制实验性高血压大鼠的VSMC增殖,与HSP70及P53的调控有关。
The effects of captopril on proliferation of vascular smooth muscle cells (VSMC) and expres- sion of heat stress protein (HSP70) and antioncogene P53 in experimnetal hypertensive rats were determined by using ~3H-thymidine (~3H-TdR) incorporation, electron microscopy, immunohistochemistry and in situ hy- bridization. After administration of captopril, morphological changes of VSMC was antagonized, and blood presure and ~3H-TdR were significantly reduced (P<0. 01). Futhermore, captopril could reverse the en- hanced expression of HSP70 and HSP70 mRNA (P<0. 01), reduce expression of antioncogene P53 (P< 0.05) in experimental hypertensive rats. Our results suggested that captopril might inhibit proliferation of VSMC in experimental hypertensive rats, which was related with the modulation of HSP70 and P53.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
1997年第S1期20-23,共4页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
国家卫生部科研基金(No 94-1-132)
湖北省自然科学基金(No 94J076)
