Anti-fatigue effects of oral supplementation with reduced Coenzyme Q10 in adults and elderly dogs

Anti-fatigue effects of oral supplementation with reduced Coenzyme Q10 in adults and elderly dogs
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口服补充还原型辅酶 Q10 对成年犬和老年犬的抗疲劳作用

DOI:
10.1111/asj.12328
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发表时间:
2014
期刊:
J Anim Vet Advan
影响因子:
--
通讯作者:
Uetake Katsuji.
Uetake Katsuji.
中科院分区:
--
文献类型:
--
作者:
Suzuki Takehito.;Kitada Natsumi.;Sakamoto Hirokazu.;Kubo Hiroshi;Takizawa Tatsuya;Uetake Katsuji.

文献摘要

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研究了米根霉(Rhizopus oryzae/U-1)水提物(RU)对四氯化碳(CCl_4)诱导的大鼠肝损伤的保护作用。为探讨RU的作用,大鼠在口服CCl4(12 5 mg/kg体重)造成肝损伤前,分别以10或10 0 mg/kg体重灌胃RU,连续10d。(I)RU可使血清乳酸脱氢酶(LDH)、丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)活性显著降低,而CCl4可使LDH、ALT和AST活性升高。(2)RU(10 0 mg/kg)可使肝细胞5-溴-2‘-脱氧尿嘧啶核苷(5-溴-2’-脱氧尿嘧啶核苷)的掺入在CCl_4处理后48 h增加。(3)肝脏组织学苏木精-伊红染色显示,RU预处理减轻了CCl4所致的损伤。(4)逆转录聚合酶链式反应分析显示,RU再处理可引起肝细胞生长因子(HGF)的一过性显著升高和胰岛素样生长因子-I(IGF-I)基因表达的持续显著增加。上述结果表明,口服RU能有效地抑制随后口服CCl4所致的肝损伤,RU诱导的IGF-I和HGF基因表达增加甚至可能部分参与了RU的生物学作用。
Hepatoprotective effects ofRhizopus oryzae/U‐1 aqueous extract (RU) were demonstrated in carbon tetrachloride (CCl4)‐induced liver‐injured rats. In order to investigate the RU effects, the rats were administered RU at a dose of 10 or 100 mg/kg of body weight for 10 days before induction of the liver injury by oral administration of CCl4(125 mg/kg body weight). (i) Pretreatment with RU caused a significant decrease in serum lactate dehydrogenase (LDH), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities that were increased by the administration of CCl4. (ii) RU pretreatment (100 mg/kg) increased 5‐bromo‐2′‐deoxyuridine incorporation at 48 h after CCl4treatment in hepatocytes. (iii) Histological hematoxylin and eosin staining of the liver showed that RU pretreatment reduced the damage induced by CCl4administration. (iv) Reverse transcriptase PCR analysis showed RU retreatment caused a transient but significant increase in hepatocyte growth factor (HGF) and a sustained and significant increase in insulin‐like growth factor‐I (IGF‐I) gene expression in hepatocytes injured by CCl4treatment. From these results, we conclude that oral pre‐administration of RU was effective to suppress liver injury induced by the subsequent oral CCl4administration, and RU‐induced increase in IGF‐I and HGF gene expression may be, even in part, involved in biological actions of RU in rats.