P38信号转导通路对蛛网膜下腔出血后迟发性脑血管痉挛的影响  

Effects of P38 Mitogen-Activated Protein Kinase Signal Transduction Pathway in Delayed Cerebral Vasospasm After Subarachnoid Hemorrhage

作　　者：余亚娟[1,2] 柯国平[1] 

机构地区：[1]武汉大学医学院人体解剖学教研室,湖北武汉430071 [2]咸宁学院医学院内科学教研室,湖北咸宁437100

出　　处：《武汉大学学报（医学版）》2009年第5期610-613,I0002,共5页Medical Journal of Wuhan University

摘　　要：目的:探讨促分裂原活化蛋白激酶P38(P38 MAPK)在兔蛛网膜下腔出血(SAH)后迟发性脑血管痉挛(CVS)中的作用。方法:35只新西兰白兔随机分为对照组(n=5),SAH组(n=10)、SAH+DMSO(n=10)、SAH+SB203580组(n=10),采用枕大池二次注血的方法建立SAH模型。分别在注血后第5天、第7天活体灌注处死,留取基底动脉标本。用免疫组织化学、测量基底动脉横截面积的方法检测P38 MAPK的表达和CVS程度的变化。结果:5 d处死的SAH组、SAH+DMSO组兔基底动脉横截面积与对照组相比有统计学意义(P<0.01),平滑肌细胞P38 MAPK的表达与对照组相比显著增强(P<0.01);5 d处死的SAH+SB203580组CVS明显缓解(P<0.01),平滑肌细胞P38 MAPK的表达减弱。结论:SAH后兔基底动脉平滑肌细胞内激活的P38 MAPK诱导了迟发性CVS的产生;SB203580能够有效的缓解基底动脉平滑肌持续性的收缩。Objective： To study the role of P38 MAPK in the development of delayed cerebral vasospasm after subarachnoid hemorrhage（SAH）.Methods： Thirty-five New Zealand white rabbits were divided randomly into four group： control（n=5）,SAH（n=10）,SAH＋DMSO（n=10）,and SAH＋SB203580（n=10） groups.The SAH model was established by using blood injection via cisternal puncture twice.The perfusion-fixation was performed respectively on the 5th and 7th day after blood-injection in vivo and the entire length of basilar artery was harvested.The degree of cerebral vasospasm was evaluated by measuring the cross-sectional area of each basilar arterial lumen,and the expression of P38 MAPK in the vascular wall was examined with immunohistochemistry.Results： In the SAH group and SAH＋DMSO group,the cross-sectional area of rabbits basilar arterial lumen on the 5th day was statistically smaller than that in the control group（P〈0.01）,and the expression of P38 MAPK in the vascular wall was statistically higher than that...更多 in the control group（P〈0.01）.The cross-sectional area of arterial lumen in the SAH＋SB203580 group on the 5th day was statistically larger than in SAH and SAH＋DMSO groups in the same period,and P38 MAPK could not be detected in the vascular smooth muscle cell layer.Conclusion： Activated P38 MAPK in rabbits smooth muscle cells after SAH could induce the development of delayed cerebral vasospasm,and P38 MAPK specific inhibitor SB203580 is able to attenuate effectively the persistent contraction of arterial smooth muscle.

关 键 词：促分裂原活化蛋白激酶P38 蛛网膜下腔出血 脑血管痉挛 信号转导 

分 类 号：R743.35[医药卫生—神经病学与精神病学]