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低氧介导的编程细胞死亡与 brojlers 木制乳房的形成有关

Xinrui Zhang¹, Tong Xing¹, Lin Zhang¹

¹College of Animal Science and Technology, Key Laboratory of Animal Origin Food Production and Safety Guarantee of Jiangsu Province, Jiangsu Collaborative Innovation Center of Meat Production and Processing, Quality and Safety Control, Nanjing Agricultural University, No. 1 Weigang, Nanjing, Jiangsu, 210095, P.R. China.

Journal of animal science and biotechnology

|June 5, 2024

概括

brojler的木乳肌病涉及到血液供应的减少和胸部大肌肉的缺氧. 这会触发被编程的细胞死亡,包括亡,自和亡,导致肌肉损伤.

科学领域:

动物科学动物科学
兽医病理学兽医病理学
分子生物学分子生物学

背景情况:

木质乳房 (WB) 肌病是商业肉中普遍存在的疾病,其特点是损伤大胸肌 (PM).
驱动WB发展的精确机制仍然不完全理解,促使人们对低氧介导的编程细胞死亡 (PCD) 进行调查.

研究的目的:

调查缺氧诱导的编程细胞死亡 (PCD) 在肉木乳房 (WB) 肌肉病变的发病过程中的作用.
为了阐明特定的PCD途径 (亡,自,亡) 激活响应低氧条件在胸部大肌肉内.

主要方法:

从对照和WB受影响的肉中对主要胸部 (PM) 肌肉进行了组织学和生物化学分析.
评估血液气体水平 (pO2,sO2,pCO2,TCO2) 以评估缺氧状况.
在mRNA和蛋白质水平上对自,亡和亡途径的关键分子标记物的评估.

主要成果:

患有WB的肉显著增加了乳腺肌肉厚度和肌纤维损伤.
在WB受影响的PM肌肉中证实了缺氧状况,其指标是毛细血管密度下降和血液气体配置的改变.
观察到自标志物 (LC3 II/I比,HIF-1α,BNIP3,Beclin1,AMPKα,ULK1) 和亡标志物 (Bax,Cytc,caspase 9,caspase 3) 的显著上调.
亡标志物 (RIP1,RIP3,MLKL) 和促炎细胞因子 (TNF-α,IL-1β,IL-6) 的表达增加表明这些PCD通路的激活.

结论:

在WB肌病症中,血液供应减少导致胸部大肌肉的缺氧.
缺氧与肌纤维内被编程的细胞死亡途径的激活密切相关,包括细胞亡,自和亡.
这些细胞事件最终导致异常的肌肉损伤和 brojlers 木制乳房的发展.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.自自是一种自的过程.肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉肉氧气过低是因为缺氧.尸体灭 (Necroptosis) 是一种死亡的过程.木制的乳房是木制的

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