动物营养学报 >

2014 , Vol. 26 >Issue 9: 2779 - 2788

DOI: https://doi.org/10.3969/j.issn.1006-267x.2014.09.041

饲料营养 Feed Science and Technology

叔丁基对苯二酚对热应激小鼠肝脏氧化损伤的缓解作用

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  • 南京农业大学动物科技学院, 南京 210095
周鑫（1988-），男，浙江金华人，博士研究生，动物营养与饲料科学专业。E-mail：zhouxin_2046@126.com

收稿日期: 2014-03-01

  网络出版日期: 2014-09-10

基金资助

国家自然科学基金（31272485）；青蓝工程；“十二五”国家科技支撑计划（2012BAD39B02）

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Tert-Butylhydroquinone: Preventive Effects on Heat Stress-Induced Oxidative Damage in Liver of Mice

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  • College of Animal Science and Technology, Nanjing Agriculture University, Nanjing 210095, China

Received date: 2014-03-01

  Online published: 2014-09-10

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摘要

本试验旨在研究叔丁基对苯二酚（tBHQ）对热应激小鼠肝脏氧化损伤的影响。试验选用50只6周龄ICR雄性小鼠随机分为2组，每组25只，tBHQ（-）组饲喂基础饲粮，tBHQ（+）组饲喂基础饲粮中添加1% tBHQ的试验饲粮。饲喂14 d后，小鼠每天进行42℃2 h热应激处理，连续8 d。在热应激之前（热应激0 d）和热应激1、2、4、8 d，每组各取5只小鼠处死，采集肝脏，测定肝脏重量和抗氧化指标，免疫组织化学方法检测转录因子E2相关因子2（Nrf2）和血红素加氧酶1（HO-1）蛋白表达，实时定量PCR法测定Nrf2及其调控表达基因的表达量。结果表明：1）tBHQ（-）组肝脏指数在热应激4 d恢复正常水平，而tBHQ（+）组在热应激2 d即恢复正常水平。2）与tBHQ（-）组相比，热应激0 d，tBHQ（+）组肝脏总超氧化物歧化酶（T-SOD）活力显著升高（P<0.05），在热应激4 d时，还原型谷胱甘肽含量以及T-SOD、铜，锌超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶活力显著降低（P<0.05）。3）热应激2 d，tBHQ（-）组比tBHQ（+）组肝脏损伤情况更为严重。4）热应激0 d，tBHQ（-）组未检测到Nrf2蛋白在肝脏组织表达，热应激后各时间点都检测到Nrf2蛋白的表达，而tBHQ（+）组在各阶段均有表达；tBHQ（-）组在热应激0、1、4和8 d都检测到HO-1蛋白的表达，而tBHQ（+）组在热应激0、1和2 d时检测到了HO-1蛋白的表达。5）与tBHQ（-）组相比，tBHQ（+）组多个Kelch样ECH相关蛋白（Keap1）-Nrf2/ARE信号通路相关基因表达量均显著升高（P<0.05）。综上所述，饲粮添加1% tBHQ对热应激造成的小鼠肝脏氧化损伤能够起到一定的缓解作用。

关键词： 叔丁基对苯二酚; 肝脏; 热应激; 氧化损伤

本文引用格式

周鑫, 黄毅, 李延森, 李春梅 . 叔丁基对苯二酚对热应激小鼠肝脏氧化损伤的缓解作用[J]. 动物营养学报, 2014 , 26(9) : 2779 -2788 . DOI: 10.3969/j.issn.1006-267x.2014.09.041

Abstract

To investigate the effects of tert-butylhydroquinone (tBHQ) on heat stress-induced oxidative damage in liver of mice, fifty six-week-old ICR male mice were divided into 2 groups with 25 mice in each group. tBHQ (-) group received a basal diet, and tBHQ (+) group received the basal diet supplemented with 1% tBHQ. After 14 days of feeding, mice were exposed to the elevated ambient temperature (42℃) daily for 2 h. During the period of 8 consecutive days, five mice in each group were sacrificed to collect liver before heat stress (0 day after heat stress) and at 1, 2, 4 and 8 days after heat stress, respectively. Liver weight and antioxidative indices were determined, transcription factor E2 related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) protein expressions in liver were determined by immunohistochemical detection, and the expressions of Nrf2 gene and Nrf2-regulated genes were analyzed by real time-PCR detection. The results showed as follows: 1) liver index of tBHQ (-) group recovered to normal level at 4 days after heat stress, while that of tBHQ (+) group recovered to normal level at 2 days after heat stress. 2) Compared with tBHQ (-) group, total superoxide dismutase (T-SOD) activity of tBHQ (+) group was significantly increased at 0 day after heat stress (P<0.05), and reduced glutathione hormone (GSH) content and the activities of T-SOD, copper, zinc-superoxide dismutase (Cu, Zn-SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) of tBHQ (+) group were significantly reduced at 4 days after heat stress (P<0.05). 3) At 2 days after heat stress, liver injury of tBHQ (-) group was more serious than that of tBHQ (+) group. 4) Nrf2 protein expression was not detected in liver at 0 day after heat stress, but it was detected at all the time points after heat stress of tBHQ (-) group and was detected at all the time points of tBHQ (+) group; HO-1 protein expression was detected in liver at 0, 1, 4 and 8 days after heat stress of tBHQ (-) group, and at 0, 1 and 2 days after heat stress of tBHQ (+) group. 5) Compared with tBHQ (-) group, multiple genes of kelch-like ECH-associated protein 1 (Keap1)-Nrf2/ARE signing pathway of tBHQ (+) group were significantly increased (P<0.05). In conclusion, dietary supplementation of 1% tBHQ can alleviate heat stress-induced oxidative damage in liver of mice.

Key words： tert-butylhydroquinone; liver; heat stress; oxidative damage

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