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首页> 外文期刊>Toxicology and Applied Pharmacology >CoQ10 protects against acetaminophen-induced liver injury by enhancing mitophagy
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CoQ10 protects against acetaminophen-induced liver injury by enhancing mitophagy

机译：CoQ10通过增强乳化物来防止乙酰氨基酚诱导的肝损伤

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Coenzyme Q10 (CoQ10), which is a key cofactor of the electron transport chain in the mitochondria has shown many beneficial effects on liver diseases. However, the mechanisms of CoQ10 protective role on the acetaminophen (APAP)-induced liver injury are elusive and unclear. In this study, we further investigated the CoQ10 therapeutic effects on APAP-overdose liver injury. C57BL/6 J mice were intraperitoneally treated with APAP to induce liver injury. CoQ10 (5 mg/kg) was given to mice at 1.5 h after APAP treatment. The results showed that hepatic CoQ10 levels were decreased during the APAP-induced hepatotoxicity and preceded serum ALT elevation. Treatment of CoQ10 significantly improved the liver injury induced by APAP. Moreover, CoQ10 treatment decreased the ROS levels and promoted the antioxidative related gene expression in APAP overdose mice. Importantly, results showed that even though CoQ10 had no effects on the mtDNA copy number and the expression of genes related to mitochondrial biogenesis, it significantly improved the mitochondrial complex I and V activities and promoted the mitophagy in APAP-overdose mice. To further authenticate mitophagy role in CoQ10-mediated improved liver injury in vivo, we administrated APAP-overdose mice with chloroquine 1 h prior to APAP treatment and found that chloroquine treatment functionally abrogated the CoQ10 protective role on APAP overdose mice. To conclude, this study provides evidence that CoQ10 activates mitophagy to protect against APAP-induced liver injury. Therefore, CoQ10 may represent a novel therapeutic option for the prevention and treatment of drug-induced liver injury.
机译：辅酶Q10（辅酶Q10）是线粒体电子传递链的关键辅因子，对肝脏疾病有许多有益作用。然而，辅酶Q10对乙酰氨基酚（APAP）诱导的肝损伤的保护作用机制尚不清楚。在本研究中，我们进一步研究了辅酶Q10对APAP过量肝损伤的治疗效果。C57BL/6J小鼠腹腔注射APAP诱导肝损伤。在APAP治疗后1.5小时，给小鼠服用辅酶Q10（5 mg/kg）。结果表明，在APAP诱导的肝毒性期间，肝脏辅酶Q10水平降低，并先于血清ALT升高。辅酶Q10治疗显著改善APAP诱导的肝损伤。此外，辅酶Q10治疗降低了APAP过量小鼠的ROS水平，并促进了抗氧化相关基因的表达。重要的是，结果表明，尽管辅酶Q10对线粒体DNA拷贝数和线粒体生物发生相关基因的表达没有影响，但它显著改善了APAP过量小鼠的线粒体复合物I和V活性，并促进了有丝分裂吞噬。在氯喹治疗小鼠之前，我们发现氯喹对CoQ10介导的肝损伤有进一步的保护作用。综上所述，本研究提供了辅酶Q10激活有丝分裂吞噬以防止APAP诱导的肝损伤的证据。因此，辅酶Q10可能是预防和治疗药物性肝损伤的一种新的治疗选择。

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