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目的 观察血管平滑肌细胞在单纯高压力作用下凋亡及其相关蛋白Bcl 2和Bax的变化 ,探讨力学因素在血管重建中的作用。 方法 应用血管体外应力培养系统 ,分别在压力 10 0mmHg和 16 0mmHg条件下培养猪颈总动脉 1、4和 7d ,新鲜血管为对照。应用TUNEL法、透射电镜等观察血管平滑肌细胞的凋亡 ;用免疫组织化学方法检测血管平滑肌细胞内Bcl 2和Bax的表达。 结果 高压力作用下 ,血管平滑肌细胞凋亡第 1d较多 ,而后逐渐减少 ;Bcl 2蛋白表达持续增强 ;Bax蛋白第 1d较多 ,而后逐渐减少。 结论 高压力可以影响血管平滑肌细胞的凋亡 ,凋亡相关蛋白Bcl 2持续增加 ,Bax先增加后减少 ,揭示高压力可能通过调节Bcl 2和Bax来调控血管平滑肌细胞的凋亡。
Objective To observe the changes of apoptosis and related proteins Bcl 2 and Bax in vascular smooth muscle cells under high pressure and explore the role of mechanical factors in vascular remodeling. Methods The vascular in vitro stress culture system was used to culture the common carotid arteries 1, 4 and 7 days under pressure of 10 0 mmHg and 160 mmHg, respectively. Fresh blood vessels were used as control. The apoptosis of vascular smooth muscle cells was observed by TUNEL and transmission electron microscopy. The expression of Bcl-2 and Bax in vascular smooth muscle cells was detected by immunohistochemistry. Results Under high pressure, the apoptosis of vascular smooth muscle cells was more on the 1st day and then gradually decreased; the expression of Bcl 2 protein continued to increase; the Bax protein was more on the 1st day and then decreased gradually. Conclusions High pressure can affect the apoptosis of vascular smooth muscle cells. The expression of Bcl-2 and Bax first increase and then decrease, suggesting that high pressure may regulate the apoptosis of vascular smooth muscle cells through regulating Bcl 2 and Bax.