Abstract：
The objective of this study was to investigate the mechanism underlying nitric oxide (NO)-induced hypoxia-inducible factor-1α (HIF-1α) and its impact on yak muscle tenderness during post-mortem aging. The Longissimus thoracis et lumborum (LTL) muscle of yak were incubated at 4 °C for 0, 3, 6, 9, 12, 24, and 72 h after treatment with 0.9% saline, NO activator, or a combination of the NO activator and an HIF-1α inhibitor. Results indicated that elevated NO levels could increase HIF-1α transcription to achieve stable expression of HIF-1α protein (P < 0.05). Additionally, elevated NO triggered HIF-1α S-nitrosylation, which further upregulated the activity of key glycolytic enzymes, increased glycogen consumption, accelerated lactic acid accumulation, and decreased pH (P < 0.05). These processes eventually improved the tenderness of yak muscle during post-mortem aging (P < 0.05). The results demonstrated that NO-induced activation of HIF-1α S-nitrosylation enhanced glycolysis during post-mortem aging and provided a possible pathway for improving meat tenderness.
摘要：
本研究的目的是研究一氧化氮（NO）诱导的缺氧诱导因子-1α（HIF-1α）的机制及其对宰后衰老牦牛肌肉压痛的影响。用0.9％盐水处理后，在4°C下孵育牦牛的胸腰长肌（LTL）肌肉0、3、6、9、12、24和72h，无活化剂,或NO激活剂和HIF-1α抑制剂的组合。结果表明，升高的NO水平可以增加HIF-1α的转录，从而实现HIF-1α蛋白的稳定表达（P<0.05）。此外,NO升高引发HIF-1αS-亚硝基化，这进一步上调了关键糖酵解酶的活性，糖原消耗增加，加速乳酸积累，pH值下降(P<0.05)。这些过程最终改善了宰后老化期间牦牛肌肉的压痛(P<0.05)。结果表明，NO诱导的HIF-1αS-亚硝基化激活可增强死后衰老过程中的糖酵解，并为改善肉嫩度提供了可能的途径。
