过氧化氢诱导的肉鸡肌肉氧化损伤机制及牛磺酸的缓解作用研究

The oxidative damage of broilers exposed to high levels of relative oxygen species (ROS) caused by oxidative stress can impair the meat quality, which blocks the healthy development of modern broiler industry. It is worth noting that many previous studies investigate the problem of oxidative damage based on one of a variety of stressors that indirectly induce the production of ROS, which results in the precise mechanism of oxidative damage in muscle of broilers remains elusive. The direct way of increasing body ROS levels could provide a new research idea for clarifying the mechanism of oxidative damage. As a highly active ROS in organism, hydrogen peroxide (H2O2) can be generated by almost all oxidative stressors. Taurine has been demonstrated to have antioxidative function. Therefore, the objective of this project is to study the responsive relationship between the change in meat quality and oxidative damage induced by high levels of ROS in muscle of broilers administrated with H2O2. Moreover, we further explore the occurrence rule of apoptosis and autophagy, and the expression regularity of NF-κB signal pathway in both in vivo and in vitro experiments to investigate the mechanism of oxidative damage induced by ROS. Then, we study alleviative effect of taurine on oxidative damage of muscle. We will clarify the molecule mechanism of H2O2-induced oxidative damage and the antioxidative function of taurine. The results will provide an important theoretical basis for alleviating broiler oxidative stress by establishing strategies for scientific management and nutrition regulation in broiler industry.

氧化应激会使肉鸡机体活性氧（ROS）水平升高，引起氧化损伤，导致肉品质下降，严重危害肉鸡产业发展。前人研究氧化损伤问题时，大都以单一应激源刺激机体间接产生ROS为前提。由于应激源性质和处理方法不同，使得氧化损伤确切机制尚不明确。采用直接增加机体ROS水平的方法可为探讨氧化损伤机制提供新思路。过氧化氢（H2O2）是机体内的高活性氧，几乎可由所有氧化应激源产生。研究表明，牛磺酸具有抗氧化性。基于此，本项目拟采用直接注射H2O2的方法，研究H2O2诱发的高浓度ROS对肉鸡肌肉氧化损伤与肉品质变化的效应关系；结合细胞培养研究H2O2诱发的高浓度ROS对肉鸡肌肉细胞凋亡与自噬发生变化规律以及NF-κB通路关键因子表达规律的影响与机制，并进一步研究牛磺酸的缓解作用。结果可揭示H2O2诱导肉鸡肌肉氧化损伤的分子机制及牛磺酸的作用效果，可为肉鸡生产中建立科学缓解氧化应激的管理与营养调控策略提供理论依据。

氧化应激会使肉鸡机体活性氧（Relative oxygen species，ROS）水平升高，引起氧化损伤，导致肉鸡生长性能和肉品质下降，危害肉鸡产业的发展。前人研究氧化损伤问题时，大都以单一应激源刺激机体间接产生ROS为前提。由于应激源性质和处理方法不同，使得氧化损伤确切机制尚不明确。采用直接增加机体ROS水平的方法可为探讨氧化损伤机制提供新思路。已有研究证实过氧化氢（H2O2）是机体内的高活性ROS，几乎可由所有氧化应激源产生。研究表明牛磺酸具有抗氧化性。本研究发现：腹腔注射2.96 mmol/kg 体重的H2O2可降低42日龄肉鸡的生长性能，并降低21日龄肉鸡肝脏的器官指数；腹腔注射H2O2降低了鸡肉品质，并降低42日龄肉鸡的相对肌肉重；腹腔注射H2O2可提高42日龄肉鸡肝脏和肌肉的ROS水平，并破坏肝脏和肌肉的组织形态，降低血清、肝脏和肌肉的抗氧化能力，并促进了氧化产物的积累，引起肉鸡机体的氧化损伤。腹腔注射2.96 mmol/kg 体重的H2O2能够通过提高Caspase因子的表达诱发肉鸡肝脏和肌肉细胞的凋亡；腹腔注射H2O2能够通过增加Beclin 1和LC3-II的表达促进肉鸡肝脏和肌肉细胞自噬的发生；腹腔注射H2O2可能通过抑制NF-κB信号通路来诱导肉鸡肝脏和肌肉细胞凋亡和自噬的发生。H2O2会引起鸡原代成肌细胞和小鼠C2C12细胞中ROS水平升高，并且能够通过抑制NF-κB信号通路介导细胞凋亡和自噬的发生，这与NF-κB因子的特异性抑制剂吡咯烷二硫代氨基甲酸盐（PDTC）的作用类似。饲喂添加0.5%的牛磺酸日粮可改善H2O2降低的肉鸡生长性能和升高的肌肉剪切力；日粮添加牛磺酸可缓解胸肌ROS升高，一定程度恢复胸肌线粒体功能，并对胸肌抗氧化能力的修复和氧化产物的清除起作用，这可能与牛磺酸下调了H2O2升高的ROS水平，通过激活NF-κB信号通路调控肉鸡胸肌细胞凋亡和自噬过程，进而起到氧化缓解的作用有关。综上，本项目揭示了H2O2诱导肉鸡肌肉氧化损伤的分子机制及牛磺酸的作用效果，为肉鸡生产中建立科学缓解氧化应激的管理与营养调控策略提供了理论依据。

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