CAJ | 학술논문

目的探讨甘珀酸对兔实验性蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)时缝隙连接蛋白43(Cx43)磷酸化表达的影响.方法建立兔二次SAH模型,脑池及静脉分别给予甘珀酸,脑血管造影及光镜观察分析基底动脉直径及形态学变化并应用Western blot检测基底动脉Cx43蛋白磷酸化表达的变化.结果 SAH组与正常组相比,脑血管造影及光镜观察结果证实基底动脉痉挛明显;痉挛动脉肇磷酸化的Cx43(P-Cx43)蛋白表达显著升高,但去磷酸化的Cx43(NP-Cx43)蛋白表达显著减少.甘珀酸脑池处理组及静脉处理组与SAH组相比,脑血管造影及光镜观察结果证实基底动脉痉挛显著减轻;痉挛动脉壁P-Cx43蛋白表达显著减少,但NP-Cx43蛋白表达显著升高.结论 SAH后,Cx43蛋白磷酸化表达发生变化,脑池或静脉给予甘珀酸能明显缓解SAH后CVS,其作用机制可能与基底动脉Cx43蛋白磷酸化表达变化有关.
목적 탐토감박산대토실험성주망막하강출혈(SAH)후뇌혈관경련(CVS)시봉극련접단백43(Cx43)린산화표체적영향.방법 건립토이차SAH모형,뇌지급정맥분별급여감박산,뇌혈관조영급광경관찰분석기저동맥직경급형태학변화병응용Western blot검측기저동맥Cx43단백린산화표체적변화.결과 SAH조여정상조상비,뇌혈관조영급광경관찰결과 증실기저동맥경련명현;경련동맥조린산화적Cx43(P-Cx43)단백표체현저승고,단거린산화적Cx43(NP-Cx43)단백표체현저감소.감박산뇌지처리조급정맥처리조여SAH조상비,뇌혈관조영급광경관찰결과 증실기저동맥경련현저감경;경련동맥벽P-Cx43단백표체현저감소,단NP-Cx43단백표체현저승고.결론 SAH후,Cx43단백린산화표체발생변화,뇌지혹정맥급여감박산능명현완해SAH후CVS,기작용궤제가능여기저동맥Cx43단백린산화표체변화유관.
Objective The study was designed to investigate the expression of Connexin43 ( Cx43) phosphorylation in the basilar arteries on cerebral vasospasm after experimental subarachnoid hemorrhage(SAH) and the effects of carbenoxolone(CBX) on CVS and Cx43 phosphorylation expression in rabbits. Method The double - hemorrhage model of SAH with injecting into the cistema magna was used. CBX was given intracistemally or intravenously. Angiography and hematoxylin and eosin staining were performed to observe the diameter and for morphological study of the basilar artery. Western blotting was used to analyze the phosphorylation expression of Cx43 protein in basilar artery. Results After SAH, arterial narrowing and morphological changes in vascular structure were significantly more than that in normal group. CBX inhibited these changes; compared to that in normal group, phosphorylated Cx43 was up - regulated, while dephosphorylated Cx43 was down - regulated in the basilar artery vessel wall after SAH. CBX successfully reversed these alterations of Cx43 phosphorylation. Conclusions The expression changes of Cx43 phosphorylation plays an important role in the pathogenesis of CVS. CBX reduces cerebral vasospasm after SAH by modulating the alterations of Cx43 phosphorylation.