摘要
目的研究衰老引起的大鼠颈总动脉血管平滑肌细胞(VSMC)收缩功能的改变,并探讨钙库操纵的钙内流(SOCE)及其组成分子Orai 1和基质相互作用因子1(STIM1)对血管收缩的调节作用。方法应用离体血管实验,通过特异性细胞内钙泵阻断剂毒胡萝卜素,清空细胞内钙库,并用维拉帕米阻断L型钙离子通道,特异性观察不同月龄大鼠VSMC中SOCE的变化;采用免疫荧光染色法检测Orai 1和STIM 1蛋白在不同月龄大鼠颈总动脉VSMC中的表达。结果与年轻大鼠相比,老年大鼠颈总动脉对60 mmol/L高钾去极化引起的收缩显著增强(P<0.05),但SOCE引起的血管收缩在高钾引起的收缩中所占百分比显著减小(P<0.05)。与年轻大鼠相比,老年大鼠VSMC中Orai 1和STIM1蛋白表达水平降低。结论与年轻大鼠相比,老年大鼠颈总动脉VSMC中SOCE显著减弱,可能与Orai 1和STIM 1蛋白表达减少有关。
Objective To investigate the changes of the contract and regulation function of Orai 1 and STIM 1 which consisted of store-operated Ca2＋ entry（SOCE） of vascular smooth muscle cells（VSMCs） from aged rat carotid artery.Methods Apply vessel experiment in vitro,VSMCs were treated by thapsigargin to deplete Ca2＋ store and verapamil to block L-type Ca2＋ channel.The changes of SOCE in VSMCs of rats with different ages were detected.The protein expression levels of Orai 1 and STIM 1 were observed by immunofluorescence method.Results Vessel tension measurement showed that 60 mmol/L KCl-induced vessel contraction of aged rat was significantlyhigher than that of young rat（P0.05）.However,the percentage of SOCE-induced vessel contraction in 60 mmol/L KCl-induced vessel contraction of aged rat was significantly smaller than that of young rat（P0.05）.Conclusion Compared with young rat,SOCE is significantly attenuated in VSMC of aged rat carotid artery,which may be caused by decreased the protein expression levels of Orai 1 and STIM 1.
出处
《安徽医科大学学报》
CAS
北大核心
2012年第2期122-126,共5页
Acta Universitatis Medicinalis Anhui
基金
国家自然科学基金(编号:30800384)
安徽医科大学博士科研资助基金(编号:XJ200913)
