卡托普利对自发性高血压大鼠血管平滑肌细胞增殖及癌基因和抑癌基因的影响

目的：观察卡托普利（CaP）对自发性高血压大鼠（SHR）血管平滑肌细胞（VSMC）增殖的作用及对原癌基因及抑癌基因的影响。方法：氚-胸腺嘧啶核苷（3H－TdR）参入，电镜，原位来交及Northernblot杂交。结果：CaP在降低SHR血压同时，能减少VSMC的线粒体，粗面内质网及3H－TdR参入量（P<0.01），并能逆转c－fos，c－myc，c－sis原癌基因mRNA表达增强（P<0.05或0.01），p53抑癌基因mRNA表达减弱（P＜0．01）。结论：Cap能抑制SHR的VSMC增殖，与癌基因调控的分子生物学机制有关。

The effects of captopril on proliferation of vascular smooth muscle cells and expression of oncogenes c-my,c-fos,c-sis and antioncogene p53 in spontaneously hypertensive rats

AIM: To determine the effects ofcaptopril on proliferation of vascular smoothmuscle cells (VSMC) and expression of onco-gene c-myc, c-fos, c-sis and antionc0gene p53 inspontaneously hypertensive rats (SHR )-METHODS: 'H-thymidine (3H-TdR ) incorpora-tion, electr0nic micr0sc0py, in situ hybridizationand Northern blot assaies were used' RE-SULTS: After administration of captopril, mor-phological change of VSMC was antagnized, andblood pressure and 3H-TdR data were signifi-cantly reduced (PwtO' Ol ). Furthermore. capto-pril could reverse the enhanced expression ofoncogene c-my c - c-.fos. c-sis (P r O' Oi> ~ O. Ol )and reduced expression of antioncogene l>53 (Prt 0.01 ) in SHR' CONCLUSIONS: (;al7toPrilmight inhibit DNA synthesis and pr0llferation ofVSMC in SHR, related with the mechanism ofmolecular biology of contr0lling oncogene'