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.

中文翻译：

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NO 诱导的缺氧诱导因子-1α 对宰后老化过程中牦牛肉嫩度的潜在影响

本研究的目的是探讨一氧化氮 (NO) 诱导缺氧诱导因子 1α (HIF-1α) 的机制及其对死后老化过程中牦牛肌肉嫩度的影响。用 0.9% 盐水、NO 激活剂或 NO 激活剂组合处理后，将牦牛的胸腰最长肌 (LTL) 肌肉在 4°C 下孵育 0、3、6、9、12、24 和 72 小时和 HIF-1α 抑制剂。结果表明，NO水平升高可以增加HIF-1α转录，实现HIF-1α蛋白的稳定表达（P < 0.05）。此外，NO升高会引发HIF-1α S-亚硝基化，进一步上调关键糖酵解酶的活性，增加糖原消耗，加速乳酸积累，降低pH值（P < 0.05）。这些过程最终改善了牦牛肌肉在宰后老化过程中的嫩度（P < 0.05）。结果表明，NO 诱导的 HIF-1α S-亚硝基化激活增强了死后老化过程中的糖酵解，并为改善肉嫩度提供了可能的途径。