摘要
目的:探讨在尾加压素Ⅱ(UⅡ)受体拮抗剂urantide干预下,UⅡ在大鼠血管平滑肌细胞(VSMC)中的表达,阐明其可能的作用机制。方法:采用贴块法对大鼠胸主动脉血管平滑肌细胞进行体外培养,实验分为正常对照组(C组)、UⅡ组(M组)、阳性药对照组(Flu组)及urantide干预组(浓度分别为1×10-10、1×10-9、1×10-8、1×10-7和1×10-6 mol·L-1),采用MTT法检测VSMC增殖活性,采用流式细胞术测定VSMC增殖指数(PI)及S期细胞分数(SPF)。结果:与正常对照组比较,UⅡ组在各时间点VSMC增殖活性均增加(P<0.01);PI及SPF明显增加(P<0.01);与UⅡ组比较,1×10-10～10-6 mol·L-1urantide组VSMC增殖活性明显降低(P<0.05或P<0.01),PI及SPF均明显减少(P<0.05或P<0.01),其中以1×10-6 mol·L-1urantide作用最明显。结论:urantide可阻断UⅡ对动脉粥样硬化(AS)主要病变细胞VSMC的促丝裂作用,本研究为临床应用urantide治疗AS提供了新的视角和实验依据。
Objective To investigate the expressions of both urotensin Ⅱ(UⅡ) and its receptor GPR14 in rat vascular smooth muscle cells(VSMC) under the intervention of urantide(UⅡ receptor antagonist),and clarify its possible mechanism.Methods The VSMC from rat thoracic aorta were cultivated in vitro with tissue explant method,and divided into normal control group(C group),UⅡ group(M group),positive control group(Flu group) and five intervention groups(10-10,10-9,10-8,10-7 and 10-6 mol·L-1 urantide).The proliferation index(PI) and S-phase cell fraction(SPF) of in vitro cultured VSMC were detected with MTT method and flow cytometry.Results Compared with C group,the VSMC proliferation was increased at each time point(P<0.01),and PI and SPF were also increased significantly(P<0.01);compared with M group,the VSMC proliferation in 10-10-10-6 mol·L-1 urantide groups were significantly decreased(P<0.05 or P<0.01),and PI and SPF were significantly reduced(P<0.05 or P<0.01),among which 10-6 mol·L-1 urautide group had the most significant effect.Conclusion Urantide can block the mitogenic effect of UⅡ on atherosclerosis(AS) of the major disease-promoting cells VSMC,providing a new perspective and experimental basis for clinical application of urantide to treat AS.
出处
《吉林大学学报（医学版）》
CAS
CSCD
北大核心
2011年第6期1079-1082,1177,共5页
Journal of Jilin University：Medicine Edition
基金
承德医学院博士基金资助课题(201102)
