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首页> 美国卫生研究院文献>other >RBC-coupled tPA Prevents Whereas tPA Aggravates JNK MAPK-Mediated Impairment of ATP- and Ca-Sensitive K Channel-Mediated Cerebrovasodilation After Cerebral Photothrombosis
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RBC-coupled tPA Prevents Whereas tPA Aggravates JNK MAPK-Mediated Impairment of ATP- and Ca-Sensitive K Channel-Mediated Cerebrovasodilation After Cerebral Photothrombosis

机译：RBC偶联的TPA可防止而TPA加剧JNK MAPK介导的ATP和CA敏感性K通道介导的脑中介质后脑介导的脑癌的损伤

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The sole Food and Drug Administration-approved treatment for acute stroke is tissue-type plasminogen activator (tPA), but tPA aggravates impairment of cerebrovasodilation during hypotension in a newborn pig photothrombotic model of stroke. Coupling to carrier red blood cells (RBC) enhances thrombolytic effects of tPA, while reducing its side effects. ATP- and Ca-sensitive K channels (Katp and Kca) are important regulators of cerebrovascular tone and mediate cerebrovasodilation during hypotension. Mitogen-activated protein kinase, a family of at least three kinases, ERK, p38, and c-Jun-N-terminal kinase (JNK), is upregulated after photothrombosis. This study examined the effect of photothrombosis on Katp- and Kca-induced cerebrovasodilation and the roles of tPA and JNK during/after injury. Photothrombosis blunted vasodilation induced by the Katp agonists cromakalim, calcitonin gene-related peptide, and the Kca agonist NS 1619, which was aggravated by injection of tPA. In contrast, both pre- or post-injury thrombosis injection of RBC-tPA and JNK antagonist SP 600125 prevented impairment of Katp- and Kca-induced vasodilation. Therefore, JNK activation in thrombosis impairs K channel-mediated cerebrovasodilation. Standard thrombolytic therapy of central nervous system ischemic disorders using free tPA poses the danger of further dysregulation of cerebrohemodynamics by impairing cation-mediated control of cerebrovascular tone, whereas RBC-coupled tPA both restores reperfusion and normalizes cerebral hemodynamics.
机译：急性中风的唯一食物和药物管理批准的治疗是组织型纤溶酶原激活剂（TPA），但TPA加剧了在新生猪中风中脑卒中的低血压期间脑疏松疏松的损害。偶联至载体红细胞（RBC）增强TPA的溶栓作用，同时降低其副作用。 ATP-和CA敏感的K通道（KATP和KCA）是脑血管间调的重要调节因子，并在低血压期间调解脑癌。丝裂剂活化蛋白激酶，至少三个激酶，ERK，P38和C-JUN-N-末端激酶（JNK）的家族在光学胶质形成后上调。本研究检测了光学凝集对KATP和KCA诱导的颅内脑致疏松和损伤期间/后/后的作用的影响。通过注射TPA加重的KATP激动剂Cromakalim，Calcitonin基因相关肽和KCA激动剂NS 1619诱导的光电诱导血管舒张。相比之下，RBC-TPA和JNK拮抗剂SP 600125的预损伤后或后损伤后血栓形成注射，防止了KATP和KCA诱导的血管舒张的损伤。因此，JNK激活血栓形成损害K通道介导的脑升沉。使用自由TPA的中枢神经系统缺血性疾病的标准溶栓治疗通过损害抗血管血管间距的阳离子介导的控制，造成脑血管动力学的进一步失调的危险，而RBC偶联的TPA均恢复再灌注并标准化脑血流动动力学。

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