Coxsackievirus B4-induced neuronal apoptosis in rat cortical cultures
Coxsackievirus B4-induced neuronal apoptosis in rat cortical cultures
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DOI：
10.1016/s0304-3940(02)00340-3
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发表时间：
2002-07-05
影响因子：
2.5
通讯作者：
Kim, DH
中科院分区：
文献类型：
--
作者：
Joo, CH;Kim, YK;Kim, DH
肠道病毒感染中枢神经系统(CNS)是免疫低下儿童和成人发病的常见和重要原因。在这项研究中，我们鉴定和表征了柯萨奇病毒B4诱导的神经元死亡。为探讨柯萨奇病毒B4(CVB4)感染大鼠中枢神经系统的病理生理机制，用柯萨奇病毒B4(CVB4)感染培养的大鼠神经元，观察细胞形态、磷脂酰丝氨酸(PS)外化以及放线菌素D和放线菌酮(CHX)对其影响。CVB4感染后24 h内可引起神经细胞死亡，而感染后16 h胞体中PS明显外化。放线菌素D或CHX可显著降低CVB4诱导的神经细胞死亡，并呈剂量依赖关系。CHX或放线菌素D也可抑制CVB4感染后发生的核固缩。然而，这些变化对zVAD-fmk的响应相对较慢。这些结果表明，CVB4诱导CHX和放线菌素D敏感，而zVAD-fmk不敏感。(C)2002年，爱思唯尔科学爱尔兰有限公司出版。
Enterovirus infections of the central nervous system (CNS) are common and important causes of morbidity in immunocompromised children and adults. In this study we identify and characterize coxsackievirus B4-induced neuronal death. To investigate the CNS pathophysiology resulting from this viral infection, cultured rat neurons were infected with coxsackievirus B4 (CVB4) and nuclear morphology, phosphatidylserine (PS) externalization, and the effects of Actinomycin D or cycloheximide (CHX) were examined. CVB4 induced neuronal cell death within 24 h while PS externalization was apparent in cell bodies 16 h after CVB4 infection. Actinomycin D or CHX significantly reduced CVB4 induced-neuronal cell death in a dose-dependent manner. Pretreatment with CHX or actinomycin D also inhibited nuclear condensation, which occurred after CVB4 infection. However, the changes were relatively unresponsive to zVAD-fmk. These results suggest that CVB4 induces CHX- and actinomycin D-sensitive, but zVAD-fmk-insensitive neuronal apoptosis. (C) 2002 Published by Elsevier Science Ireland Ltd.