Liu Ning, Zhang Bolin, Wang Shubai, Zhong Qingzhen, Sun Zewei
College of Animal Science and Technology, Jilin Agricultural University, Changchun 130118, China.
College of Animal Science and Technology, Qingdao Agricultural University, Qingdao 266109, China.
Anim Biosci. 2025 Apr;38(4):765-774. doi: 10.5713/ab.24.0418. Epub 2024 Oct 28.
Antemortem stress accelerated muscle energy consumption in postmortem muscle. The objective of our study was to investigate the regulation of guanidinoacetic acid (GAA) administration on the postmortem glycolysis and protein acetylation in postmortem muscle of antemortem stress.
Forty C57BL/6 male mice were chosen and randomly assigned to four treatment groups (A, B, C and D), each treatment consisted of 10 replicates. Mice in group B, C and D were treated with 0.05% GAA oral administration for 6 days. On the 7th day of the experiment, the mice in group A and B were injected with saline, and mice in group C and D were injected with 5-aminoimidazole-4-carboxamide1-β-D-ribofuranoside (AICAR; 50 μg/g body weight) and a combined injection with AICAR (50 μg/g body weight) and histone acetylase inhibitor II (HAT II; 185 μg/g body weight), respectively.
The results showed that the values of pH45min and pH24h of postmortem muscle in GAA administration were higher than those in the control group. However, the opposite result was observed in AICAR group. Moreover, the activities of pyruvate kinase, hexokinase and fruc-tose-2,6-diphosphatase, combined with the protein abundance of phosphorylated liver kinase, phosphorylated AMPKα2 and total acetylated protein were all decreased by GAA administration and HAT II treatment.
Taken together, adenosine 5'-monophosphate-activated protein kinase signaling and protein acetylation could mediate the regulation of GAA administration on postmortem glycolysis of antemortem stress-muscle.
生前应激会加速死后肌肉的能量消耗。本研究的目的是探讨胍基乙酸（GAA）给药对生前应激后死后肌肉糖酵解和蛋白质乙酰化的调节作用。
选取40只C57BL/6雄性小鼠，随机分为四个处理组（A、B、C和D），每个处理组有10个重复。B、C和D组小鼠口服0.05% GAA，持续6天。在实验的第7天，A组和B组小鼠注射生理盐水，C组和D组小鼠分别注射5-氨基咪唑-4-甲酰胺-1-β-D-呋喃核糖苷（AICAR；50μg/g体重）以及AICAR（50μg/g体重）与组蛋白乙酰化酶抑制剂II（HAT II；185μg/g体重）的联合注射剂。
结果显示，给予GAA后死后肌肉的pH45min和pH24h值高于对照组。然而，在AICAR组观察到相反的结果。此外，给予GAA和HAT II处理后，丙酮酸激酶、己糖激酶和果糖-2,6-二磷酸酶的活性，以及磷酸化肝激酶、磷酸化AMPKα2和总乙酰化蛋白的蛋白质丰度均降低。
综上所述，5'-单磷酸腺苷激活的蛋白激酶信号传导和蛋白质乙酰化可介导GAA给药对生前应激肌肉死后糖酵解的调节作用。
