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目的本研究将模拟失重大鼠整体实验与离体血管灌流培养实验相结合,重点观察在不同跨壁压条件下整合素(integrin)及其关联的信号转导分子的表达、激活、募集等变化规律。方法整体实验:大鼠尾部悬吊法模拟失重4周(SUS组),并设同步对照组(CON组)。观察模拟失重对大鼠IntegrinαV、Integrinβ3、Src、ERK和p-ERK蛋白表达的影响。血管培养实验:建立可以控制流量、压力的血管培养系统。结果悬吊组与对照组相比,颈总动脉IntegrinαV、Src和p-ERK蛋白表达显著上调(P<0.05),而Integrinβ3和ERK蛋白表达无显著性差异。在血管培养实验中,与常压组(80 mm Hg)相比,高压(150 mm Hg)灌流可引起IntegrinαV、Integrinβ3、Src、ERK和p-ERK升高(P<0.05),但在3 d的高压灌流期间,如每天1 h使灌流压降为80 mm Hg,则上述改变即可被部分改善,即IntegrinαV、Integrinβ3和Src蛋白表达恢复至接近常压(80 mm Hg)水平。结论跨壁压分布变化是失重引起动脉区域性重构的始动原因;但每日只要短时间使其恢复常压,血管重构及整合素下游分子的变化即可被部分防止。
OBJECTIVE: To investigate the effects of different transmembrane pressures on the expression and activation of integrin and its related signal transducers in vitro and in vivo. law. Methods The whole experiment: The rat tail suspension method simulated the weightlessness for 4 weeks (SUS group), and set the synchronous control group (CON group). To observe the effects of simulated weightlessness on the expression of IntegrinαV, Integrinβ3, Src, ERK and p-ERK in rats. Vascular culture experiment: Establish a vascular culture system that can control the flow and pressure. Results Compared with the control group, the expression of IntegrinαV, Src and p-ERK in the common carotid artery was significantly increased (P <0.05), while there was no significant difference in the expression of Integrinβ3 and ERK. In the vascular culture experiment, high pressure (150 mm Hg) perfusion induced an increase in IntegrinαV, Integrinβ3, Src, ERK and p-ERK compared with the normal pressure group (80 mm Hg) During the hyperbaric perfusion, if the perfusion pressure was reduced to 80 mm Hg at 1 h per day, the above changes could be partially ameliorated: the expression of IntegrinαV, Integrinβ3 and Src returned to near normal (80 mm Hg) levels. Conclusions The change of transmural pressure distribution is the cause of regional arterial remodeling caused by weightlessness. However, it can be partially prevented by resuming the normal pressure in a short time every day, vascular remodeling and molecular changes downstream of integrin.