Coenzyme Q10 (CoQ10) is a component of the mitochondrial electron transport chain and regarded as a strong anti-oxidant agent. In this study, we focused on the mechanistic insights involved in the hepato-protective effects of CoQ10 against hepatic ischemia reperfusion (IR) injury. Our results revealed that CoQ10 significantly improved hepatic dysfunctions and oxidative stress caused by IR injury. Interestingly, as compared to IR subjected rat, CoQ10 inhibited apoptosis by marked down-regulation of both Bax and PUMA genes while the level of Bcl-2 gene was significantly increased. Moreover, CoQ10 up-regulated PI3K, Akt and mTOR protein expressions while it inhibited the expression of both GSK-3β and β-catenin. Additionally, CoQ10 restored oxidant/antioxidant balance via marked activated Nrf-2 protein as well as up-regulation of both Sirt-1 and FOXO-3 genes. Moreover, CoQ10 strongly inhibited inflammatory response through down-regulation of NF-κB-p65 and decrease both JAK1 and STAT-3 protein expressions with a subsequent modulating circulating inflammatory cytokines. Furthermore, histopathological analysis showed that CoQ10 remarkably ameliorated the histopathological damage induced by IR injury. Taken together, our results suggested and proved that CoQ10 provided a hepato-protection against hepatic IR injury via inhibition of apoptosis, oxidative stress, inflammation and their closed related pathways.

中文翻译：

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辅酶Q10通过调节Bax / Bcl-2 / PUMA和Nrf-2 / FOXO-3 / Sirt-1信号通路来保护肝脏细胞免受缺血再灌注诱导的细胞凋亡和氧化应激。

辅酶Q10（CoQ10）是线粒体电子传输链的组成部分，被视为一种强抗氧化剂。在这项研究中，我们集中于参与CoQ10对肝缺血再灌注（IR）损伤的肝保护作用的机制研究。我们的结果表明，辅酶Q10可显着改善由IR损伤引起的肝功能障碍和氧化应激。有趣的是，与接受IR的大鼠相比，辅酶Q10通过显着下调Bax和PUMA基因来抑制细胞凋亡，而Bcl-2基因的水平却显着增加。此外，辅酶Q10上调PI3K，Akt和mTOR蛋白表达，同时抑制GSK-3β和β-catenin的表达。另外，CoQ10通过显着活化的Nrf-2蛋白以及Sirt-1和FOXO-3基因的上调来恢复氧化剂/抗氧化剂的平衡。此外，辅酶Q10通过下调NF-κB-p65强烈抑制炎症反应，并降低JAK1和STAT-3蛋白表达，并随后调节循环炎症细胞因子。此外，组织病理学分析表明辅酶Q10明显减轻了IR损伤引起的组织病理学损伤。综上所述，我们的结果表明并证明，辅酶Q10通过抑制细胞凋亡，氧化应激，炎症及其封闭的相关途径，为肝脏IR损伤提供了肝脏保护作用。CoQ10通过下调NF-κB-p65强烈抑制炎症反应，并降低JAK1和STAT-3蛋白表达，并随后调节循环炎症细胞因子。此外，组织病理学分析表明辅酶Q10明显减轻了IR损伤引起的组织病理学损伤。综上所述，我们的结果表明并证明CoQ10通过抑制细胞凋亡，氧化应激，炎症及其封闭的相关途径，为肝脏IR损伤提供了肝脏保护。CoQ10通过下调NF-κB-p65强烈抑制炎症反应，并降低JAK1和STAT-3蛋白表达，并随后调节循环炎症细胞因子。此外，组织病理学分析表明辅酶Q10明显减轻了IR损伤引起的组织病理学损伤。综上所述，我们的结果表明并证明CoQ10通过抑制细胞凋亡，氧化应激，炎症及其封闭的相关途径，为肝脏IR损伤提供了肝脏保护。