Coenzyme Q10 Protects Astrocytes from Ultraviolet B-Induced Damage Through Inhibition of ERK 1/2 Pathway Overexpression

Coenzyme Q10 Protects Astrocytes from Ultraviolet B-Induced Damage Through Inhibition of ERK 1/2 Pathway Overexpression
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DOI:
10.1007/s11064-019-02812-6
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发表时间:
2019-05
影响因子:
4.4
通讯作者:
Qi Zhao;Yan-mei Ma;L. Jing;Tianyang Zheng;Hai-Feng Jiang;P. A. Li;Jian-zhong Zhang
Qi Zhao;Yan-mei Ma;L. Jing;Tianyang Zheng;Hai-Feng Jiang;P. A. Li;Jian-zhong Zhang
中科院分区:
医学3区
文献类型:
--
作者:
Qi Zhao;Yan-mei Ma;L. Jing;Tianyang Zheng;Hai-Feng Jiang;P. A. Li;Jian-zhong Zhang

文献摘要

相似文献

细胞外信号调节激酶1/2(ERK 1/2)信号通路的过表达导致诱导氧化应激的活性氧(ROS)的过度产生。辅酶Q10(CoQ 10)清除ROS并保护细胞免受氧化应激。本研究旨在探讨辅酶Q10对星形胶质细胞氧化损伤的保护作用是否通过调节ERK 1/2通路实现。选择紫外线B(UVB)照射作为诱导氧化应激的工具。小鼠星形胶质细胞在UVB之前用10 μg/ml和25 μg/ml CoQ 10处理24小时,并在UVB期间和UVB后24小时维持。通过活细胞计数和MTT转化试验评价细胞活力。使用荧光探针测量ROS产生。采用免疫细胞化学和/或Western blotting检测p-ERK 1/2、ERK 1/2、p-PKA、PKA的表达。结果表明,UVB照射使活细胞数减少。这种损伤作用与ROS的积累和p-ERK 1/2和p-PKA的升高有关。用25 μg/ml的辅酶Q10处理显著增加了活细胞的数量,并阻止了UVB诱导的ROS、p-ERK 1/2和p-PKA的增加。结论:抑制PKA-ERK 1/2信号通路可能是辅酶Q10保护星形胶质细胞免受UVB诱导的氧化损伤的重要机制之一。
Overexpression of extracellular signal-regulated kinase ½ (ERK ½) signaling pathway leads to overproduction of reactive oxygen species (ROS) which induces oxidative stress. Coenzyme Q10 (CoQ10) scavenges ROS and protects cells against oxidative stress. The present study was designed to examine whether the protection of Coenzyme Q10 against oxidative damage in astrocytes is through regulating ERK 1/2 pathway. Ultraviolet B (UVB) irradiation was chosen as a tool to induce oxidative stress. Murine astrocytes were treated with 10 μg/ml and 25 μg/ml of CoQ10 for 24 h prior to UVB and maintained during UVB and 24 h post-UVB. Cell viability was evaluated by counting viable cells and MTT conversion assay. ROS production was measured using fluorescent probes. Levels of p-ERK 1/2, ERK 1/2, p-PKA, PKA were detected using immunocytochemistry and/or Western blotting. The results showed that UVB irradiation decreased the number of viable cells. This damaging effect was associated with accumulation of ROS and elevations of p-ERK 1/2 and p-PKA. Treatment with CoQ10 at 25 μg/ml significantly increased the number of viable cells and prevented the UVB-induced increases of ROS, p-ERK 1/2, and p-PKA. It is concluded that suppression of the PKA-ERK 1/2 signaling pathway may be one of the important mechanisms by which CoQ10 protects astrocytes from UVB-induced oxidative damage.