Neuroprotective Effect of Ginkgolide B on Bupivacaine-Induced Apoptosis in SH-SY5Y Cells
Neuroprotective Effect of Ginkgolide B on Bupivacaine-Induced Apoptosis in SH-SY5Y Cells
复制标题
银杏内酯B对布比卡因诱导的SH-SY5Y细胞凋亡的神经保护作用
DOI：
10.1155/2013/159864
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发表时间：
2013-01-01
影响因子：
--
通讯作者：
Xu, Shi-yuan
中科院分区：
文献类型：
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作者：
Li, Le;Zhang, Qing-guo;Xu, Shi-yuan
局部麻醉剂的使用是常规和有效的。然而，许多人也知道激活神经毒性途径。我们测试了银杏内酯B（GB），银杏叶的活性成分，对局部麻醉剂布比卡因引起的ROS介导的神经毒性的神经保护作用。用不同浓度的布比卡因单独或与GB预孵育后处理SH-SY 5 Y细胞。用GB预处理增加SH-SY 5 Y细胞活力，并减弱细胞内ROS积累、凋亡、线粒体功能障碍和ER应激。GB抑制布比卡因诱导的线粒体去极化和线粒体复合物I和III的抑制，并增加裂解的caspase-3和Htra 2的表达，这是强烈的指示激活的细胞凋亡与随之而来的Grp 78，caspase-12 mRNA，蛋白质和ER应激的表达增强。GB还改善了布比卡因诱导的线粒体和ER损伤的超微结构变化。这些结果暗示布比卡因诱导的ROS依赖性线粒体，ER功能障碍和细胞凋亡，这可以通过其抗氧化性能的GB衰减。
Local anesthetics are used routinely and effectively. However, many are also known to activate neurotoxic pathways. We tested the neuroprotective efficacy of ginkgolide B (GB), an active component of Ginkgo biloba, against ROS-mediated neurotoxicity caused by the local anesthetic bupivacaine. SH-SY5Y cells were treated with different concentrations of bupivacaine alone or following preincubation with GB. Pretreatment with GB increased SH-SY5Y cell viability and attenuated intracellular ROS accumulation, apoptosis, mitochondrial dysfunction, and ER stress. GB suppressed bupivacaine-induced mitochondrial depolarization and mitochondria complex I and III inhibition and increased cleaved caspase-3 and Htra2 expression, which was strongly indicative of activation of mitochondria-dependent apoptosis with concomitantly enhanced expressions of Grp78, caspase-12 mRNA, protein, and ER stress. GB also improved ultrastructural changes indicative of mitochondrial and ER damage induced by bupivacaine. These results implicate bupivacaine-induced ROS-dependent mitochondria, ER dysfunction, and apoptosis, which can be attenuated by GB through its antioxidant property.