Protective effects of sesamin and sesarnolin on murine BV-2 microglia cell line under hypoxia
Protective effects of sesamin and sesarnolin on murine BV-2 microglia cell line under hypoxia
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DOI：
10.1016/j.neulet.2004.05.073
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发表时间：
2004-08-26
影响因子：
2.5
通讯作者：
Jeng, KCG
中科院分区：
文献类型：
--
作者：
Hou, RCW;Wu, CC;Jeng, KCG
测试芝麻素和芝麻林素保护BV-2小胶质细胞免于缺氧诱导的细胞死亡的能力。这些抗氧化剂剂量依赖性地减少缺氧诱导的乳酸脱氢酶（LDH）的释放和二氯荧光素（DCF）敏感的活性氧（ROS）的产生。进一步研究了它们对缺氧诱导的细胞死亡中的信号通路丝裂原活化蛋白激酶（MAPK）和半胱天冬酶-3的影响。细胞外信号调节蛋白激酶（ERK 1/2）、c-jun氨基末端激酶（JNK）和p38 MAPK在缺氧过程中被激活。芝麻素或芝麻林减少caspase-3和MAPK的激活与BV-2细胞在缺氧条件下LDH释放减少密切相关。此外，它们在缺氧条件下保存BV-2细胞中的超氧化物歧化酶（SOD）和过氧化氢酶活性。总之，这些结果表明，芝麻抗氧化剂的机制涉及抑制MAPK途径和细胞凋亡，通过清除ROS在缺氧应激BV-2细胞。(C)2004爱思唯尔爱尔兰有限公司保留所有权利。
Sesamin and sesamolin were tested for their ability to protect BV-2 microglia from hypoxia-induced cell death. These antioxidants dose-dependently reduced hypoxia-induced lactate dehydrogenase (LDH) release and dichlorofluorescein (DCF)-sensitive reactive oxygen species (ROS) production. Their effects on signaling pathway mitogen-activated protein kinases (MAPKs) and caspase-3 in hypoxia-induced cell death were further examined. Extracellular signal-regulated protein kinases (ERK1/2), c-jun NH2-terminal kinase (JNK), and p38 MAPKs were activated during hypoxia. The sesamin or sesamolin reduced caspase-3 and MAPK activation correlated well with diminished LDH release in BV-2 cells under hypoxia. Furthermore, they preserved superoxide dismutase (SOD) and catalase activities in BV-2 cells under hypoxia. Taken together, these results indicate that the mechanism of sesame antioxidants involves inhibition of MAPK pathways and apoptosis through scavenging of ROS in hypoxia-stressed BV-2 cells. (C) 2004 Elsevier Ireland Ltd. All rights reserved.