Hydrogen Sulfide Protects against Chemical Hypoxia-Induced Injury via Attenuation of ROS-Mediated Ca(2+) Overload and Mitochondrial Dysfunction in Human Bronchial Epithelial Cells.
Hydrogen Sulfide Protects against Chemical Hypoxia-Induced Injury via Attenuation of ROS-Mediated Ca(2+) Overload and Mitochondrial Dysfunction in Human Bronchial Epithelial Cells.
复制标题
硫化氢通过减弱人支气管上皮细胞中 ROS 介导的 Ca2 超载和线粒体功能障碍来防止化学缺氧引起的损伤
DOI：
10.1155/2018/2070971
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发表时间：
2018
影响因子：
--
通讯作者：
Qin XQ
中科院分区：
文献类型：
--
作者：
Liu CX;Tan YR;Xiang Y;Liu C;Liu XA;Qin XQ
缺氧/缺血引起的氧化应激导致活性氧（reactive oxygen species，ROS）过多和抗氧化剂相对不足。气道上皮细胞作为抵抗环境污染物和过敏性刺激的最初屏障，易受氧化应激的影响。近年来，硫化氢（H2S）的抗氧化作用引起了人们的广泛关注。因此，在本研究中，我们探讨了H2S对CoCl 2诱导的16 HBE 140-细胞损伤的影响。采用CCK-8细胞计数试剂盒检测CoCl_2对16 HBE_（14）~（o-）细胞活力的影响，并检测不同剂量CoCl_2对16 HBE_（14）~（o-）细胞活性氧水平的影响（100-1000 μmol/L）CoCl2用荧光探针DCFH-DA测定了16 HBE 140-细胞中缺氧的浓度，CoCl 2以剂量依赖性方式急剧增加ROS含量，NaHS（作为H2S的供体）抑制ROS的增加。用钙离子荧光探针Fura-2/AM和荧光染料Rh 123分别测定16 HBE 140-细胞内钙离子浓度（[Ca ~（2+）]i）和线粒体膜电位（MMP）。此外，我们用Hoechst 33342检测了16 HBE 140-细胞的凋亡。结果表明，CoCl 2可有效地增加细胞内Ca 2+内流，降低MMP，加重细胞凋亡，而NaHS则可逆转上述作用。这些结果表明，H2S可以减轻CoCl 2诱导的缺氧损伤，通过减少ROS的钙离子内流和MMP耗散的拮抗作用。
Oxidative stress induced by hypoxia/ischemia resulted in the excessive reactive oxygen species (ROS) and the relative inadequate antioxidants. As the initial barrier to environmental pollutants and allergic stimuli, airway epithelial cell is vulnerable to oxidative stress. In recent years, the antioxidant effect of hydrogen sulfide (H2S) has attracted much attention. Therefore, in this study, we explored the impact of H2S on CoCl2-induced cell injury in 16HBE14o- cells. The effect of CoCl2 on the cell viability was detected by Cell Counting Kit (CCK-8) and the level of ROS in 16HBE14o- cells in response to varying doses (100–1000 μmol/L) of CoCl2 (a common chemical mimic of hypoxia) was measured by using fluorescent probe DCFH-DA. It was shown that, in 16HBE14o- cells, CoCl2 acutely increased the ROS content in a dose-dependent manner, and the increased ROS was inhibited by the NaHS (as a donor of H2S). Moreover, the calcium ion fluorescence probe Fura-2/AM and fluorescence dye Rh123 were used to investigate the intracellular calcium concentration ([Ca2+]i) and mitochondria membrane potential (MMP) in 16HBE14o- cells, respectively. In addition, we examined apoptosis of 16HBE14o- cells with Hoechst 33342. The results showed that the CoCl2 effectively elevated the Ca2+ influx, declined the MMP, and aggravated apoptosis, which were abrogated by NaHS. These results demonstrate that H2S could attenuate CoCl2-induced hypoxia injury via reducing ROS to perform an agonistic role for the Ca2+ influx and MMP dissipation.
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影响因子：
3.7
作者：
Bucchieri F;Marino Gammazza A;Pitruzzella A;Fucarino A;Farina F;Howarth P;Holgate ST;Zummo G;Davies DE
通讯作者：
Davies DE
影响因子：
4.3
作者：
Lüneburg N;Siques P;Brito J;Arriaza K;Pena E;Klose H;Leon-Velarde F;Böger RH
通讯作者：
Böger RH
影响因子：
--
作者：
Hsu SW;Chang TC;Wu YK;Lin KT;Shi LS;Lee SY
通讯作者：
Lee SY
影响因子：
3.7
作者：
Gao, Shenglan;Li, Wenting;Tang, Xiaoqing
通讯作者：
Tang, Xiaoqing
硫化氢通过改善线粒体功能障碍和抑制皮层神经元中 ROS 介导的 caspase-3 通路来防止 OGD/R 诱导的细胞凋亡
影响因子：
4.2
作者：
Luo, Yougen;Yang, Xifei;Wu, Jiyun
通讯作者：
Wu, Jiyun