CAJ | 학술논문

目的研究自发性高血压大鼠平滑肌细胞增殖特性.方法采用细胞培养、核酸杂交、酶联免疫法及反义核酸技术检测内皮素对自发性高血压大鼠和Wi star-kyoto大鼠的血管平滑肌细胞增殖、碱性成纤维细胞生长因子表达的影响,并进行对比分析.结果内皮素-1诱导了血管平滑肌细胞的增殖,且诱导了其碱性成纤维细胞生长因子的表达.但是内皮素-1对自发性高血压大鼠血管平滑肌细胞增殖作用显著高于对Wistar-kyoto大鼠血管平滑肌细胞, 对它们碱性成纤维细胞生长因子表达作用也不相同,作用峰值分别为8倍和3 .5倍,且到达峰值时间不同,分别为8h和4h.且反义核酸对内皮素-1诱导的自发性高血压大鼠血管平滑肌细胞增殖的抑制作用(80%)显著强于对内皮素-1诱导的Wistar-kyoto大鼠血管平滑肌细胞增殖的抑制作用(40%)(P<0.01).结论内皮素-1在自发性高血压大鼠平滑肌细胞增殖中具有重要作用,碱性成纤维细胞生长因子可能介导该作用.
목적연구자발성고혈압대서평활기세포증식특성.방법채용세포배양、핵산잡교、매련면역법급반의핵산기술검측내피소대자발성고혈압대서화Wi star-kyoto대서적혈관평활기세포증식、감성성섬유세포생장인자표체적영향,병진행대비분석.결과내피소-1유도료혈관평활기세포적증식,차유도료기감성성섬유세포생장인자적표체.단시내피소-1대자발성고혈압대서혈관평활기세포증식작용현저고우대Wistar-kyoto대서혈관평활기세포, 대타문감성성섬유세포생장인자표체작용야불상동,작용봉치분별위8배화3 .5배,차도체봉치시간불동,분별위8h화4h.차반의핵산대내피소-1유도적자발성고혈압대서혈관평활기세포증식적억제작용(80%)현저강우대내피소-1유도적Wistar-kyoto대서혈관평활기세포증식적억제작용(40%)(P<0.01).결론내피소-1재자발성고혈압대서평활기세포증식중구유중요작용,감성성섬유세포생장인자가능개도해작용.
Objective To study the features of vascular smooth muscle cell (VSMC) proliferation induce d by endothelin-1 (ET-1). Methods VSMCs of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats were cultu red and treated with ET-1. Basic fibroblast growth factor (bFGF) gene express ion was measured using both Northern blot and an enzyme-linked immunoassay. Results ET-1 resulted in an increase in bFGF transcripts at 8-24 h; bFGF levels were si gnificantly higher in VSMCs treated with ET-1 than in those not treated. Howev er, VSMCs gro wth responses in SHR and WKY were different. Smooth muscle cells of SHR were h yper-responsive to ET-1. Maximal bFGF mRNA levels were elevated 3.5-fold at 4 h of stimulation in WKY and 8-fold at 8h in SHR4. Moreover, the proliferatio n of VSMCs induced by ET-1 was inhibited by antisense phosphorothioate oligodeo xynucleotides (10 μmol/L AS-bFGF) but not sense bFGF oligomers at the same con centrations, being reduced by 80% in SHR and 40% in WKY vs control, respectively . Furthermore, the effect of AS-bFGF oligomers on SHR SMC proliferation is sig nificantly greater than on WKY SMC proliferation. Conclusion ET-1 may be required for exaggerated vascular growth responses in SHR and bFGF may be involved.