首页> 外文会议>Asian Society for Mitochondrial Research and Medicine >Protective Effect of -Keto-β-Methyl-n-Valeric Acid on BV-2 Microglia under Hypoxia or Oxidative Stress
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Protective Effect of -Keto-β-Methyl-n-Valeric Acid on BV-2 Microglia under Hypoxia or Oxidative Stress

机译:-Keto-β-甲基 - N- valeric酸对缺氧或氧化应激下BV-2微胶质的保护作用

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The -ketoglutarate dehydrogenase complex (KGDHC) is a mitochondrial enzyme in the TCA cycle. Inhibition of KGDHC activity by -keto-β-methyl-n-valeric acid (KMV) is associated with neuron death. However, the effect of KMV in microglia is unclear. Therefore, we investigated the effect of KMV on BV-2 microglial cells exposed to hypoxia or oxidative stress. The results showed that KMV (1-20 mM) enhanced the cell viability under hypoxia. KMV dose-dependently reduced ROS and LDH releases from hypoxic BV-2 cells. KMV also reduced ROS production and enhanced the cell viability under H_2O_2 but failed to reduce the SIN-1 and sodium nitroprusside (SNP) toxicity. KMV also reduced caspase-3 and -9 activation under stress. These results suggest that KMV protects BV-2 cells from stress and acts by reducing ROS production through inhibition of KDGHC.
机译:-Ketoglutarate脱氢酶复合物(KGDHC)是TCA循环中的线粒体酶。通过-Keto-β-甲基-N-戊酸(KMV)抑制KGDHC活性与神经元死亡有关。然而,MIMV在微胶质细胞中的影响尚不清楚。因此,我们研究了KMV对暴露于缺氧或氧化应激的BV-2微胶质细胞的影响。结果表明,KMV(1-20毫米)增强了缺氧下的细胞活力。与缺氧BV-2细胞依赖性降低了缺氧和LDH释放的KMV。 KMV还减少了ROS生产,并在H_2O_2下增强了细胞活力,但未降低SIN-1和硝普钠(SNP)毒性。 KMV还减少了CASSPASE-3和-9在应力下的激活。这些结果表明,通过抑制KDGHC来降低ROS生产,普公司免受压力的影响,并通过降低ROS产生来保护BV-2细胞。

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