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首页> 外文会议>Asian Society for Mitochondrial Research and Medicine >Oxidative Toxicity in BV-2 Microglia Cells: Sesamolin Neuroprotection of H_2O_2 Injury Involving Activation of p38 Mitogen-Activated Protein Kinase
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Oxidative Toxicity in BV-2 Microglia Cells: Sesamolin Neuroprotection of H_2O_2 Injury Involving Activation of p38 Mitogen-Activated Protein Kinase

机译：BV-2微胶质细胞中的氧化毒性：H_2O_2损伤的SESAMOLIN神经保护损伤涉及P38丝裂原激活蛋白激酶的激活

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Reactive oxygen species (ROS) has been proposed to play a pathogenic role in neuronal injury. Sesame antioxidants that inhibit lipid peroxidation and regulate cytokine production may suppress ROS generation. In this study, we focused on the effect of sesamolin on H_2O_2-induced neurotoxicity and ROS production in the murine microglial cell line BV-2. Results indicate that the H_2O_2 elicited BV-2 cell death in a concentration- and time-dependent manner. ROS generation in BV-2 cells was time-dependently increased by the H_2O_2 treatment. Sesamolin reduced ROS generation in BV-2 cells. p38 mitogen-activated protein kinase (MAPK) and caspase-3 were also activated in BV-2 cells under H_2O_2 stress. Sesamolin was able to inhibit H_2O_2-induced p38 MAPK and caspase-3 activation and cell death. In addition, sesamolin preserved superoxide dismutase and catalase activities in BV-2 cells under H_2O_2 stress. In conclusion, sesamolin protects microglia against H_2O_2-induced cell injury and this protective effect was accompanied by its inhibition of p38 MAPK and caspase-3 activation and ROS production.
机译：已经提出了活性氧物种（ROS）在神经元损伤中发挥病原作用。抑制脂质过氧化和调节细胞因子产生的芝麻抗氧化剂可以抑制ROS产生。在这项研究中，我们专注于Sesamolin对鼠微胶质细胞系BV-2中H_2O_2诱导的神经毒性和ROS产生的影响。结果表明H_2O_2以浓度和时间依赖的方式引发了BV-2细胞死亡。通过H_2O_2处理时间依赖于BV-2细胞中的ROS生成。芝麻蛋白在BV-2细胞中减少了ROS生成。在H_2O_2应力下，在BV-2细胞中也在BV-2细胞中激活P38丝裂原激活的蛋白激酶（MAPK）和Caspase-3。 Sesamolin能够抑制H_2O_2诱导的P38 MAPK和Caspase-3活化和细胞死亡。此外，在H_2O_2应力下，SESAMOLIN在BV-2细胞中保存过氧化物歧化酶和过氧化氢酶活性。总之，芝麻菌素保护小胶质细胞免受H_2O_2诱导的细胞损伤，并且这种保护作用伴随其抑制P38 MAPK和Caspase-3活化和ROS生产。

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