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熊去氧胆酸对热应激小鼠肝损伤的保护作用 被引量:3

Ursodeoxycholic Acid Ameliorates Heat Stress-induced Liver Injury in Mice
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摘要 目的:研究熊去氧胆酸(Ursodeoxycholic acid,UDCA)缓解热应激肝损伤的作用及其机制。方法:选择55只C57BL/6小鼠,随机分为空白对照组、模型组和UDCA处理组(包括低、中、高剂量组)。空白组与模型组按照0.1 m L/10 g·b·w灌胃0.5%羧甲基纤维素钠溶液,UDCA处理组分别按照20、40、80 mg/kg剂量灌胃UDCA,连续灌胃7 d,每天灌胃结束后在相同时间(12∶00~14∶00)将小鼠置于42℃恒温培养箱2 h,试验期间,小鼠自由采食和饮水。第7 d热应激结束后处死小鼠,分离肝脏,测定肝组织中丙二醛(Malondialdehyde,MDA)含量、超氧化物歧化酶(Superoxide dismutase,SOD)活力和还原性谷胱甘肽(Glutathione,GSH)含量变化以及Nrf2(Nuclear factor erythroid 2-related factor 2)蛋白和Keap1(Kelch-like ECH-associated protein-1)蛋白的表达。结果:(1)40 mg/kg、80 mg/kg UDCA可显著或极显著降低小鼠肝脏MDA含量,同时增加GSH含量和SOD活力;(2)40 mg/kg、80 mg/kg UDCA显著增加Nrf2蛋白的表达,且显著降低Keap1蛋白的表达。结论:UDCA对热应激小鼠肝损伤具有一定保护作用,具有应用前景。 Objective: To study the effect of ursodeoxycholic acid(UDCA) protective effect on heat stress-induced liver injury in mice. Methods: The model of oxidative stress was established by heat stress(HS). Fiftyfive C57 BL/6 mice were randomly divided into 5 groups: blank control group,model group,low dose group,middle dose group and high dose group. Blank group and model group were treated according to 0. 1 m L/10 g·b·w intragastric 0. 5% sodium carboxymethyl cellulose solution,the other groups were donc in accordance with the 20,40,80 mg/kg dose of UDCA,continuous intragastric administration for 7 d,Then mice were placed in a constant temperature incubator(temperature 42 ℃,relative humidity 60%) for 2 h at the same time(12∶ 00-14∶ 00). During 7 days of heat stress,the mice had free access to food and water. The contents of malondialdehyde(MDA),superoxide dismutase(SOD) and glutathione(GSH) in liver tissue were determined by the end of the7 th day,and the expression of Nrf2(nuclear factor erythroid 2-related factor 2) protein and Keap1(Kelch-like ECH-associated protein-1) protein were measured by western blotting. Results:(1) 40 mg/kg,80 mg/kg UDCA significantly decreased liver MDA levels in mice,and increased the GSH amount and SOD activity.(2) 40 mg/kg and 80 mg/kg UDCA significantly increased the expression of Nrf2,and significantly decreased the expression of Keap1. Conclusion: UDCA has a protective effect on liver injury induced by heat stress in mice.
作者 李磊 王守开 张乐 孙克诚 张文雪 丁艳梅 杨书敏 刘畅 LI Lei;WANG Shou-kai;ZHANG Le;SUN Ke-cheng;ZHANG Wen-xue;DING Yan-mei;YANG Shu-min;LIU Chang(College of Animal Science,Anhui Science and Technology Universit)
出处 《安徽科技学院学报》 2017年第6期6-9,共4页 Journal of Anhui Science and Technology University
基金 安徽省教育厅高校自然科学研究重点项目(KJ2017A503 KJ2017A504) 安徽科技学院引进人才项目(ZRC2014447) 安徽科技学院重点学科建设项目(AKZDXK2015A04) 安徽科技学院大学生创新研究项目(16XCX08) 安徽省大学生创新创业训练计划项目(201610879025 2017S10879044 2017S10879045)
关键词 熊去氧胆酸 热应激 氧化应激 NRF2 Ursodeoxycholic acid Heat stress Oxidative stress Nrf2
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