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燕麦(Avena sativa L.)提取物的补充可减轻小鼠模型中酒精引起的急性肝损伤。

Supplementation of oat (Avena sativa L.) extract abates alcohol-induced acute liver injury in a mouse model.

机构信息

Pharmacology and Toxicology Division, CSIR-Indian Institute of Chemical Technology (IICT), Hyderabad 500 007, India; Academy of Scientific and Innovative Research (AcSIR), CSIR-HRDC Campus, Sector 19, Kamla Nehru Nagar, Ghaziabad, Uttar Pradesh 201 002, India.

Pharmacology and Toxicology Division, CSIR-Indian Institute of Chemical Technology (IICT), Hyderabad 500 007, India.

出版信息

Nutr Res. 2018 Jun;54:80-92. doi: 10.1016/j.nutres.2018.04.002. Epub 2018 Apr 6.

DOI:10.1016/j.nutres.2018.04.002
PMID:29914670
Abstract

Dietary supplementation of oats has been associated with reduced risk of cardiovascular disease, diabetes, and gastrointestinal disorders. The role of oat extract as prophylactic in treating acute liver injury is not thoroughly established. We, therefore, hypothesized that oat extract would exert protective effect against alcohol-induced acute liver injury in a mouse model. To test this hypothesis, male C57BL/6 mice were pretreated with phenolic-enriched ethyl acetate (EA) fraction of oats (prepared by fractionating aqueous ethanolic extract with solvents of increasing polarity) at dosages of 125 and 250 mg kg d for 12 consecutive days. Acute liver injury was induced by administering 5 doses of 50% ethanol intragastrically (10 g/kg body weight) to mice at an interval of 12 hours. The alcohol-induced liver injury was evaluated by measuring serum levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, antioxidant parameters, mitochondrial function, and histology of liver tissue. Our results demonstrated that pretreatment with EA fraction at 250 mg kg d significantly (P < .001 for aspartate aminotransferase, alanine aminotransferase, and thiobarbituric acid-reactive species and P < .01 for lactate dehydrogenase and nitrites) reduced the levels of liver injury markers and significantly (P < .001 for glutathione reductase and glutathione S-transferase; P < .01 for catalase, superoxide dismustase, and vitamin C; P < .05 for reduced glutathione and NAD(P)H quinone dehydrogenase 1) increased the levels of antioxidant defenses. Furthermore, EA-pretreated mice showed mechanistic inhibition of nuclear factor κB signaling pathway through decreased phosphorylation and degradation of IκBα. We conclude that phenolic-enriched EA fraction of oats has immense potential to serve as dietary intervention against alcohol-induced liver damage.

摘要

燕麦的膳食补充与降低心血管疾病、糖尿病和胃肠道疾病的风险有关。燕麦提取物作为预防急性肝损伤的作用尚未得到充分证实。因此,我们假设燕麦提取物在小鼠模型中会对酒精诱导的急性肝损伤发挥保护作用。为了验证这一假设,雄性 C57BL/6 小鼠连续 12 天每天用 125 和 250mg/kg 的剂量预先用富含酚的乙酸乙酯(EA)燕麦提取物处理(通过用溶剂的极性递增对水乙醇提取物进行分级分离制备)。通过每隔 12 小时给小鼠灌胃 5 次 50%乙醇(10g/kg 体重)来诱导急性肝损伤。通过测量血清丙氨酸转氨酶、天冬氨酸转氨酶、乳酸脱氢酶、抗氧化参数、线粒体功能和肝组织学来评估酒精性肝损伤。我们的结果表明,250mg/kg 的 EA 级分预处理显著(天冬氨酸转氨酶、丙氨酸转氨酶和硫代巴比妥酸反应性物质的 P <.001,乳酸脱氢酶和亚硝酸盐的 P <.01)降低了肝损伤标志物的水平,并显著(谷胱甘肽还原酶和谷胱甘肽 S-转移酶的 P <.001;过氧化氢酶、超氧化物歧化酶和维生素 C 的 P <.01;还原型谷胱甘肽和 NAD(P)H 醌氧化还原酶 1 的 P <.05)增加了抗氧化防御水平。此外,EA 预处理的小鼠表现出核因子 κB 信号通路的机制抑制,通过减少 IκBα 的磷酸化和降解。我们得出结论,富含酚的 EA 燕麦提取物具有作为膳食干预剂对抗酒精性肝损伤的巨大潜力。

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