Coenzyme Q10 protects astrocytes from ROS-induced damage through inhibition of mitochondria-mediated cell death pathway.
Coenzyme Q10 protects astrocytes from ROS-induced damage through inhibition of mitochondria-mediated cell death pathway.
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辅酶 Q10 通过抑制线粒体介导的细胞死亡途径保护星形胶质细胞免受 ROS 诱导的损伤
DOI:
10.7150/ijbs.10174
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发表时间:
2015
影响因子:
9.2
通讯作者:
Li PA
中科院分区:
文献类型:
--
作者:
Jing L;He MT;Chang Y;Mehta SL;He QP;Zhang JZ;Li PA
Coenzyme Q10 (CoQ10) acts by scavenging reactive oxygen species to protect neuronal cells against oxidative stress in neurodegenerative diseases. The present study was designed to examine whether CoQ10 was capable of protecting astrocytes from reactive oxygen species (ROS) mediated damage. For this purpose, ultraviolet B (UVB) irradiation was used as a tool to induce ROS stress to cultured astrocytes. The cells were treated with 10 and 25 μg/ml of CoQ10 for 3 or 24 h prior to the cells being exposed to UVB irradiation and maintained for 24 h post UVB exposure. Cell viability was assessed by MTT conversion assay. Mitochondrial respiration was assessed by respirometer. While superoxide production and mitochondrial membrane potential were measured using fluorescent probes, levels of cytochrome C (cyto-c), cleaved caspase-9, and caspase-8 were detected using Western blotting and/or immunocytochemistry. The results showed that UVB irradiation decreased cell viability and this damaging effect was associated with superoxide accumulation, mitochondrial membrane potential hyperpolarization, mitochondrial respiration suppression, cyto-c release, and the activation of both caspase-9 and -8. Treatment with CoQ10 at two different concentrations started 24 h before UVB exposure significantly increased the cell viability. The protective effect of CoQ10 was associated with reduction in superoxide, normalization of mitochondrial membrane potential, improvement of mitochondrial respiration, inhibition of cyto-c release, suppression of caspase-9. Furthermore, CoQ10 enhanced mitochondrial biogenesis. It is concluded that CoQ10 may protect astrocytes through suppression of oxidative stress, prevention of mitochondrial dysfunction, blockade of mitochondria-mediated cell death pathway, and enhancement of mitochondrial biogenesis.
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DOI:
10.1126/science.1222381
发表时间:
2012-07-20
期刊:
Science (New York, N.Y.)
影响因子:
--
作者:
Tsai HH;Li H;Fuentealba LC;Molofsky AV;Taveira-Marques R;Zhuang H;Tenney A;Murnen AT;Fancy SP;Merkle F;Kessaris N;Alvarez-Buylla A;Richardson WD;Rowitch DH
通讯作者:
Rowitch DH
影响因子:
2.6
作者:
Littarru, Gian Paolo;Tiano, Luca
通讯作者:
Tiano, Luca
影响因子:
7.7
作者:
Vincent, AM;Olzmann, JA;Russell, JW
通讯作者:
Russell, JW
影响因子:
9
作者:
通讯作者:
--
影响因子:
6.2
作者:
Gosejacob, Dominic;Dublin, Pavel;Theis, Martin
通讯作者:
Theis, Martin