Neuroprotective effects of hydrogen sulfide on sodium azide-induced oxidative stress in PC12 cells.
Neuroprotective effects of hydrogen sulfide on sodium azide-induced oxidative stress in PC12 cells.
复制标题
硫化氢对叠氮化钠诱导的 PC12 细胞氧化应激的神经保护作用。
DOI：
10.3892/ijmm.2017.3227
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发表时间：
2018-01
影响因子：
5.4
通讯作者：
Tao L
中科院分区：
文献类型：
--
作者：
Gao C;Chang P;Yang L;Wang Y;Zhu S;Shan H;Zhang M;Tao L
阿尔茨海默病（AD）是最常见的神经退行性疾病，占所有痴呆病例的>50%。叠氮化钠（NaN 3）通过与血红素辅因子不可逆结合并选择性降低存在于死后AD脑中的复合物IV活性来抑制细胞色素氧化酶。先前的数据表明，硫化氢（H2S），第三种内源性气体介质，对神经元损伤具有保护作用。因此，假设H2S可能能够抑制过量的活性氧（ROS），从而保护免受氧化应激和细胞死亡。在本研究中，观察到NaN 3处理（20、30和50 mmol/l）后12 h，细胞活力以浓度依赖性方式降低。在用30 mM NaN 3处理后12 h观察到细胞活力降低（至51±3%）。NaN 3处理还导致线粒体膜电位降低，脂质过氧化（丙二醛的过量产生）增加，并增加caspase-3的蛋白表达水平。H2S（200 μmol/l）预处理可抑制NaN 3介导的细胞凋亡，其抗凋亡作用部分依赖于抑制ROS的产生。本研究的结果表明，H2S通过抗氧化和抗凋亡机制对NaN 3诱导的神经毒性产生神经保护作用。因此，本研究的结果表明，暴露于NaN 3后，基于H2S的神经元损伤预防和治疗可能有很好的前景。
Alzheimer's disease (AD) is the most common neurodegenerative disorder, responsible for >50% of all dementia cases. Sodium azide (NaN3) inhibits cytochrome oxidase by irreversibly binding to the heme cofactor and selectively reducing the complex IV activity, which is present in post-mortem AD brains. Previous data demonstrated that hydrogen sulfide (H2S), the third endogenous gaseous mediator, exerted protective effects against neuronal damage. Therefore, it was hypothesized that H2S may be able to scavenge excess reactive oxygen species (ROS), thereby protecting against oxidative stress and cell death. In the present study, it was observed that cell viability decreased in a concentration-dependent manner 12 h after NaN3 treatment (20, 30 and 50 mmol/l). A decrease in cell viability (to 51±3%) was observed 12 h after treatment with 30 mM NaN3. NaN3 treatment also led to decreased mitochondrial membrane potential, increased lipid peroxidation (excessive production of malondialdehyde), and increased the protein expression levels of caspase-3. Pretreatment with H2S (200 μmol/l) attenuated NaN3-mediated apoptosis, and the anti-apoptotic action of H2S was partially dependent on suppressing the production of ROS. The findings of the present study suggested that H2S exerted a neuroprotective effect against NaN3-induced neurotoxicity through mechanisms related to anti-oxidation and anti-apoptosis. Therefore, the findings of the present study suggest there may be a promising future for H2S-based preventions and therapies for neuronal damage following exposure to NaN3.
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影响因子：
4.8
作者：
Kimura, Y;Kimura, H
通讯作者：
Kimura, H
影响因子：
4.7
作者：
Gadalla MM;Snyder SH
通讯作者：
Snyder SH
影响因子：
2.7
作者：
Lutton, JD;Moonga, BS;Dempster, DW
通讯作者：
Dempster, DW
DOI：
10.3390/molecules191016146
发表时间：
2014-10-09
期刊：
Molecules (Basel, Switzerland)
影响因子：
--
作者：
Kimura H
通讯作者：
Kimura H
DOI：
10.3233/jad-160726
发表时间：
2017
期刊：
Journal of Alzheimer's disease : JAD
影响因子：
--
作者：
Cai Q;Tammineni P
通讯作者：
Tammineni P