摘要
采用内皮素建立培养的血管平滑肌细胞增殖模型。用氚-胸腺嘧啶核苷（［3H］－TdR）参入法，流式细胞术，免疫细胞化学及NorthemBlot杂交方法，观察卡托普利（Cap）对VSMC增殖的作用及对生长因子PDGF－B，bFGF及其相关癌基因c－sis，c－myc表达的影响。结果发现：Cap能逆转内皮素所致的［3H］－TdR参入量增多，阻止血管平滑肌细胞由静止期（G0／G1期）进入DNA合成期（S期）和有丝分裂（G2／M期），并能逆转内皮素引起的PDGF—B，bFGF抗原，c－sis，c－mycmRNA表达增强。提示：aop有抑制血管平滑肌细胞增殖作用，与生长因子及癌基因调控的分子生物学机制有关。
In order to determine the effects of captopril on endothelin (ET) - stimulated proliferation of vascular smooth muscle cells (VSMC) and expression of growth factor PDGF-B, bFGF and oncogene c-sis, c-myc, the experimental models of proliferation of cultured porcine aortic smooth muscle cells induced by ET were established,and 3H - thymidine ([3H] - TdR) incorporation, flow cytometry, immunohistochemistry and Northern Blot assaies were used. The results showed that captopril may drop [3H] - TdR data increased by ET and hold-back VSMC from static phase (G0/G1) to DNA synthetic phase (S) and mitotic phase (G2/M) Furthermore, captopril could reverse the enhanced expression of antigen PDGF - B, bFGF and reduced expression of oncogene c-sis,cmyc induced by ET. These results suggested that captopril might inhibit DNA synthesis and proliferation of VSMC, related with the mechanism of molecular biology Of controlling growth factors and oncogene.
出处
《心肺血管病杂志》
CAS
1998年第4期280-282,共3页
Journal of Cardiovascular and Pulmonary Diseases
基金
国家教委优秀年轻教师基金
湖北省自然科学基金
关键词
卡托普利
内皮素
血管平滑肌细胞
生长因子
Captopril
Endothelin
Vascular smooth muscle cells
Growth factor
Oncogene
