摘要
环氧合酶-2(cyclooxygenase-2,COX-2)是催化花生四烯酸转化为前列腺素的限速酶,广泛参与脑创伤、缺血诱导的神经元损伤、炎症反应及神经变性性疾病等。COX-2在神经病理学中的作用与神经元的突触变化有关。增强或抑制COX-2表达可增强或抑制兴奋性谷氨酸能神经元的神经传递和长时程增强(LTP),这些效应由COX-2的主要产物前列腺素E2(PGE2)及其受体亚型EP2所介导。因此,阐明COX-2在突触信号中的作用机制将有助于设计新的药物来预防、治疗及减轻神经源性炎症相关的神经紊乱性疾病。
Cyclooxygenase-2 （COX-2） is a rate-limiting enzyme converting arachidonic acid to prostaglandins （PGs）, which is a key messenger in traumatic brain injury- and ischemia-induced neuronal damage and in neuroinflammation. COX-2 is implicated in the pathogeneses of neurodegenerative diseases. Growing evidence implies that the contribution of COX-2 to neuropathology is associated with its involvement in synaptic alteration. Elevation or inhibition of COX-2 has been shown to enhance or suppress excitatory glutamatergic neurotransmission and long-term potentiation （LTP）. These events arc mainly mediated via PGE2, the predominant reaction product of COX-2, and the PGE2 subtype 2 receptor （EP2）. Thus, elucidation of COX-2 in synaptic signaling may provide a mechanistic basis for designing new drugs aimed at preventing, treating or alleviating neuroinflammation-associated neurological disorders.
出处
《生理科学进展》
CAS
CSCD
北大核心
2009年第4期317-320,共4页
Progress in Physiological Sciences
