摘要
目的:观察模拟失重大鼠胸主动脉收缩功能的变化及Rho相关的蛋白激酶(Rho-associated protein kinase,ROCK)表达的改变,并探讨二者之间的关系。方法:以尾部悬吊4周建立模拟失重大鼠模型并观察模拟失重对胸主动脉的主要生理的影响。采用离体血管环功能实验检测大鼠胸主动脉的收缩反应性变化;通过蛋白印迹技术检测大鼠胸主动脉ROCK II蛋白的表达。结果:与对照组相比,悬吊组氯化钾、苯肾上腺素诱导的大鼠胸主动脉收缩功能均明显增强(P<0.05)。用ROCK特异性抑制剂Y-27632孵育1 h后,两组胸主动脉的收缩反应均显著降低至同一水平,两组间无统计学差异。蛋白印迹结果显示,悬吊组ROCK II的表达增加。结论:ROCK表达的改变可能在模拟失重大鼠胸主动脉收缩功能增强中发挥重要作用,去除ROCK的作用可消除模拟失重大鼠与正常大鼠胸主动脉收缩功能的差异。
AIM：To investigate the vasoconstrictive responsiveness of thoracic aorta and the expression of Rho-associated protein kinase（ROCK） and to explore the relationship between altered ROCK and changed vasoconstriction of thoracic aorta induced by simulated microgravity in rats.METHODS： Four-week tail-suspended（SUS） rats were adopted as the animal models to simulate the main physiological influence on thoracic aorta due to microgravity.Tissue bath was used to measure arterial vasoreactivity and Western blot was applied to detect expression of ROCK II in thoracic aorta.RESULTS： Compared with those in control group,KCl-and phenylephrine-induced contractions both significantly increased in SUS and ROCK-specific inhibitor Y-27632 significantly reduced the aortic contractions induced by both agonists to a similar lower level.Western blot analysis showed that ROCK II expression was significantly upregulated in thoracic aorta in SUS.CONCLUSION： Altered expression and activity of ROCK may play important roles in the increased vasoconstriction of thoracic aorta induced by simulated microgravity in rats.Differences of the thoracic aortic vasoconstriction between simulated microgravity and normal rats could be eliminated by inhibition of ROCK.
出处
《心脏杂志》
CAS
2012年第6期677-680,共4页
Chinese Heart Journal
基金
国家自然科学基金资助(30971423
30871218)
