API0134对血管平滑肌细胞增殖和血小板源生长因子B链、碱性纤维母细胞生长因子及相关癌基因表达的影响  

Effects of API0134 on Proliferation of Vascular Smooth Muscle Cells and Expression of Platelet Derived Growth Factor-B Chain, Basic Fibroblast Growth Factor, c-sis and c-myc

作　　者：熊一力[1] 王宏伟[1] 赵华月[1] 

机构地区：[1]同济医科大学同济医院心内科,武汉430030

出　　处：《中国动脉硬化杂志》1997年第2期95-98,共4页Chinese Journal of Arteriosclerosis

基　　金：国家自然科学基金!39470859;湖北省自然科学基金!94J081

摘　　要：为探讨API0134防治冠状动脉粥样硬化和腔内成形术后再狭窄的作用机制，采用内皮素诱导建立培养的血管平滑肌细胞增殖模型，用氚标胸腺嘧啶脱氧核苷掺入法、流式细胞术、免疫细胞化学检测及Northernblot方法，观察了API0134对血管平滑肌细胞增殖的作用及对血小板源生长因子B链、碱性纤维母细胞生长因子及其相关癌基因C－sis和C－mpc表达的影响。结果发现，API0134能逆转内皮素所致的氚标胸腺嘧啶脱氧核苷掺入量增多（对照组为499±92，内皮素组为617±98，API0134组为506±102），阻止血管平滑肌细胞由静止期（G0／G1期；对照组为72％，内皮素组为50％，API0134组为60％）进入DNA合成期（S期；三组分别为26％、36％和30％）和有丝分裂期（G2／M期，三组分别为2％、14％和4％），并能逆转内皮素引起的血小板源生长因子B链、碱性纤维母细胞生长因子抗原、c－sis和c－mpc的mRNA表达增强。提示API0134有抑制血管平滑肌细胞增殖的作用，这种作用与生长因子及癌基因调控的分子生物学机制有关。Aim To determine the effects of API0l34 on en-dothelin (ET)-stimulated proliferation of vascularsmooth muscle cells (VSMC ) and expression ofgrowth factor, such as platelet derived growth factor(PDGF-B ) and basic fibrob1ast growth factor(bFGF), and oncogene c-sis and c-myc.Methods The experimental models of proliferationof cultured porcine aortic smooth muscle cells inducedby ET were established, and 3H-thymidine (3H-TdR ) incorporation, flow cytometry, immunohistochemistry and Northern blot assaies were used.Results API0134 may drop 3H-TdR data in-creased by ET and hold-back VSMC from static phase(G,/G, ) to DNA synthetic phase (S) and mitoticphase (G2/M ). Furthermore, API0134 could re-verse the enhanced expression of antigen PDGF-B,bFGF and reduced expression of oncogene c-sis and c-myc induced by ET.Conclusion API0134 might inhibit DNA synthesisand proliferation of VSMC, related to the mechanismof molecular biology of controlling growth factors andoncogene.

关 键 词：中药 API0134 血管平滑肌细胞 生长因子 药理学 

分 类 号：R285.5[医药卫生—中药学]