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Protective effects of Coenzyme Q10 against sevoflurane‐induced cognitive impairment through regulating apolipoprotein E and phosphorylated Tau expression in young mice
International Journal of Developmental Neuroscience ( IF 1.7 ) Pub Date : 2020-06-13 , DOI: 10.1002/jdn.10041 Man Yang 1, 2 , Hong Tan 3 , Kai Zhang 1, 2 , Naqi Lian 1, 2 , Yang Yu 1, 2 , Yonghao Yu 1, 2
International Journal of Developmental Neuroscience ( IF 1.7 ) Pub Date : 2020-06-13 , DOI: 10.1002/jdn.10041 Man Yang 1, 2 , Hong Tan 3 , Kai Zhang 1, 2 , Naqi Lian 1, 2 , Yang Yu 1, 2 , Yonghao Yu 1, 2
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Children with multiple exposures to anesthesia and surgery may be more likely to develop learning disability. Coenzyme Q10 (CoQ10) was reported to reduce the multiple sevoflurane treatment induced cognitive deficiency in 6-day old young mice. However, its specific mechanisms have not yet been found. This research aimed to reveal the role of ApoE in the pathogenesis of cognitive deficiency caused by sevoflurane anesthesia and the protective mechanism of CoQ10 in a multiple sevoflurane treatment model of young mice. The mice were randomly divided into 4 groups: Control + corn oil, Sevoflurane + corn oil, Control + CoQ10 and Sevoflurane + CoQ10. Sevoflurane group mice were anesthetized with 3% sevoflurane and 60% oxygen 2 hours a day for 3 days, while control group mice received only 60% oxygen. Mice received intraperitoneal injection of 50mg/kg CoQ10 or the same volume of corn oil 30 min before inhalation of oxygen or sevoflurane for 3 days. Mice received sevoflurane anesthesia or control treatment from the 6th to 8th day after birth. The cortex and hippocampus were harvested on the 8th day. The ATP, MMP, ApoE mRNA, total ApoE, ApoE fragments, Aβ1-40, Aβ1-42, Tau5, AT8 and PHF levels were detected. The Morris water maze (MWM) tests were performed from P30 to p36 after anesthesia or control treatment. The results indicated that the injection of CoQ10 ahead of sevoflurane treatment could reversed the anesthesia induced energy deficiency, mitochondrial dysfunction, ApoE and its fragments expression, Aβ1-42 generation, Tau phosphorylation and cognitive impairment in young mice. These data reveal that the ApoE and its fragments enhancement may play an important role in the pathogenesis of cognitive deficiency caused by sevoflurane anesthesia. CoQ10 could reduce ApoE expression by improving energy replenishment and mitochondrial functions, thereby alleviating sevoflurane-induced brain damage and cognitive impairment.
中文翻译：
辅酶 Q10 通过调节载脂蛋白 E 和磷酸化 Tau 表达对幼鼠七氟醚诱导的认知障碍的保护作用
多次接触麻醉和手术的儿童可能更容易出现学习障碍。据报道，辅酶 Q10 (CoQ10) 可减少 6 天大的年轻小鼠因多次七氟醚治疗引起的认知缺陷。但其具体机制尚未发现。本研究旨在揭示ApoE在七氟醚麻醉所致认知缺陷发病机制中的作用以及辅酶Q10在七氟醚多治疗幼鼠模型中的保护机制。将小鼠随机分为4组：对照+玉米油、七氟醚+玉米油、对照+辅酶Q10和七氟醚+辅酶Q10。七氟醚组小鼠每天2小时用3%七氟醚和60%氧气麻醉，连续3天，而对照组小鼠只接受60%氧气。小鼠在吸入氧气或七氟醚前 30 分钟腹腔注射 50mg/kg CoQ10 或等体积的玉米油，持续 3 天。小鼠在出生后第 6 天至第 8 天接受七氟醚麻醉或对照治疗。在第8天收获皮质和海马。检测ATP、MMP、ApoE mRNA、总ApoE、ApoE片段、Aβ1-40、Aβ1-42、Tau5、AT8和PHF水平。在麻醉或对照治疗后从 P30 到 p36 进行莫里斯水迷宫 (MWM) 测试。结果表明，在七氟醚治疗前注射辅酶Q10可以逆转麻醉诱导的能量不足、线粒体功能障碍、ApoE及其片段表达、Aβ1-42产生、Tau磷酸化和认知障碍。这些数据表明，ApoE 及其片段增强可能在七氟醚麻醉引起的认知缺陷的发病机制中起重要作用。CoQ10 可以通过改善能量补充和线粒体功能来降低 ApoE 的表达，从而减轻七氟醚引起的脑损伤和认知障碍。
更新日期：2020-06-13
中文翻译：
辅酶 Q10 通过调节载脂蛋白 E 和磷酸化 Tau 表达对幼鼠七氟醚诱导的认知障碍的保护作用
多次接触麻醉和手术的儿童可能更容易出现学习障碍。据报道，辅酶 Q10 (CoQ10) 可减少 6 天大的年轻小鼠因多次七氟醚治疗引起的认知缺陷。但其具体机制尚未发现。本研究旨在揭示ApoE在七氟醚麻醉所致认知缺陷发病机制中的作用以及辅酶Q10在七氟醚多治疗幼鼠模型中的保护机制。将小鼠随机分为4组：对照+玉米油、七氟醚+玉米油、对照+辅酶Q10和七氟醚+辅酶Q10。七氟醚组小鼠每天2小时用3%七氟醚和60%氧气麻醉，连续3天，而对照组小鼠只接受60%氧气。小鼠在吸入氧气或七氟醚前 30 分钟腹腔注射 50mg/kg CoQ10 或等体积的玉米油，持续 3 天。小鼠在出生后第 6 天至第 8 天接受七氟醚麻醉或对照治疗。在第8天收获皮质和海马。检测ATP、MMP、ApoE mRNA、总ApoE、ApoE片段、Aβ1-40、Aβ1-42、Tau5、AT8和PHF水平。在麻醉或对照治疗后从 P30 到 p36 进行莫里斯水迷宫 (MWM) 测试。结果表明，在七氟醚治疗前注射辅酶Q10可以逆转麻醉诱导的能量不足、线粒体功能障碍、ApoE及其片段表达、Aβ1-42产生、Tau磷酸化和认知障碍。这些数据表明，ApoE 及其片段增强可能在七氟醚麻醉引起的认知缺陷的发病机制中起重要作用。CoQ10 可以通过改善能量补充和线粒体功能来降低 ApoE 的表达，从而减轻七氟醚引起的脑损伤和认知障碍。
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