摘要:
为探讨宰后成熟过程中牛肉嫩化是否依赖抗凋亡蛋白(Bcl-2),不同部位牛肉嫩度是否存在显著差异,本文通过测定在牛肉宰后成熟过程中,Bcl-2、促凋亡蛋白(Bax)和细胞凋亡酶表达量等指标,并分析其与牛肉剪切力值的关系,最终确定Bcl-2和Bax相对含量对牛肉嫩化的作用机制。在宰后2~12 h,前躯肱三头肌(TB)、中躯背最长肌(ML)和后躯半膜肌(SM)的Bax/Bcl-2相对含量以及细胞凋亡酶(Caspase-3、Caspase-8、Caspase-9)活力均显著上升(p<0.05),宰后6~48 h,剪切力下降极显著(p<0.01)。研究表明,牛肉宰后嫩化依赖于线粒体途径和死亡受体途径,Bcl-2蛋白通过介导Caspases级联反应对牛肉嫩度进行调控。Bax/Bcl-2相对含量的升高导致Cyt-C从线粒体释放到细胞质,启动Caspase级联反应,激活Caspase-3,水解肌原纤维蛋白引发细胞凋亡,最终导致在宰后48 h内牛肉嫩度不断提高,且ML嫩度优于TB和SM。
Abstract:
This study investigated whether beef tenderization during post-mortem ripening depends on anti-apoptotic protein(Bcl-2)and whether there is a significant difference in beef tenderness among different parts. In this paper,the Bcl-2,pro-apoptotic protein(Bax)and apoptotic enzyme expression levels were measured during the post-mortem maturity of beef,and the relationship between it and the shear force value of beef was analyzed. The mechanism of the relative content of Bcl-2 and Bax on beef tenderization was finally determined. At 2~12 h postmortem,the relative contents of Bax/Bcl-2 and the activities of apoptosis enzyme(Caspase-3,Caspase-8 and Caspase-9)in anterior triceps brachii muscle(TB),midbrain longissimus muscle(ML),hindquarters semimembrane muscle(SM)increased significantly(p<0.05),shear force decreased significantly(p<0.01)at 6~48 h after slaughter. The study pointed out that the tenderness of beef depends on the mitochondrial pathway and the death receptor pathway. The Bcl-2 protein regulates the tenderness of beef through Caspases cascade reaction. The increase of the relative content of Bax/Bcl-2 leads to the release of Cyt-C from mitochondria to the cytoplasm,initiates the Caspase cascade,activates Caspase-3 to hydrolyze myofibrillar protein,and triggers apoptosis. As a result,the tenderness of beef continued to increase within 48 h after slaughter,and the tenderness of ML was better than that of TB and SM.
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