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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 investigate the role of mitogen-activated protein kinase P38 (P38 MAPK) in delayed cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) in rabbits. Methods: 35 New Zealand white rabbits were randomly divided into control group (n = 5), SAH group (n = 10), SAH + DMSO group (n = 10) and SAH + SB203580 group Blood injection method to establish SAH model. On the 5th day and the 7th day after the injection of blood, the animals were sacrificed and the basilar artery specimens were collected. The expression of P38 MAPK and the degree of CVS were detected by immunohistochemistry and basal artery cross-sectional area. Results: The basilar artery cross-sectional area of SAH group and SAH + DMSO group after 5-day treatment was significantly higher than that of control group (P <0.01), and the expression of P38 MAPK in smooth muscle cells was significantly increased compared with control group (P < 0.01). The CVS of SAH + SB203580 group that was sacrificed on day 5 was significantly relieved (P <0.01), and the expression of P38 MAPK in smooth muscle cells was weakened. CONCLUSIONS: P38 MAPK activated in basilar artery smooth muscle cells of rabbit after SAH induces the production of delayed CVS. SB203580 can effectively relieve the persistent contraction of basilar artery smooth muscle.