Skeletal muscle injuries are prone to induce fatigue, decreased resistance and imbalances in the body. Although OVA has biological effects such as promoting tissue development and immunomodulation, its impact on repairing skeletal muscle injuries has been rarely reported. In this study, a mouse model of muscle injury was constructed and found that OVA significantly increased muscle weight, muscle thickness, and exercise capacity in muscle-injured mice. Meanwhile, OVA improved the morphology of muscle tissues by reducing serum levels of UN, CK, and LDH, as well as decreasing the levels of inflammatory factors IL-1β, TNF-α, and IL-6, respectively. In addition, transcriptomic and metabolomic analyses revealed that OVA could enhance muscle tissue morphology by upregulating the PI3K-Akt signaling pathway and improving amino acid metabolism through the upregulation of Col11a2, Ccn2, Thbs1, Tnc, Klf2, Bcl2l1, Adh3a1, and Rsad1. The study provided a theoretical foundation for understanding the molecular mechanisms in OVA-aided muscle injury repair.

Related research findings indicated that the hardness of the tail meat from red swamp crayfish (Procambarus clarkii) increased when responding to cold stress during the transportation. However, the effect of low temperature on crayfish muscle was still at the phenotype level, there were few studies on the molecular mechanism of crayfish muscle response to cold stress. The effect of cold stress on the tail meat of crayfish during simulated transportation (control and low temperature stress for 12 h (LT_12), 24 h (LT_24) and 36 h (LT_36) at 4 ℃) were investigated by integrated transcriptome and proteomics. The results showed that the hardness of crayfish meat increased after cold stress. Gene ontology (GO) analysis showed that differentially expressed genes (DEGs) and differentially expressed proteins (DEPs) of crayfish coping with cold stress were mainly involved in metabolism and glycolysis. Kyoto Encyclopedia of Genes and Genomes (KEGG) metabolic analysis found that the metabolic response to cold stress included changes in amino acids such as valine and isoleucine. Low temperature activated glycolysis and amino acid metabolism pathway as well as peroxisome pathway to maintain body balance. The significant increase in the expression of cytoskeletal protein-actin related genes such as β-actin and ACT1 might cause the increase of muscle hardness under stress.