Abstract
ABSTRACT Objective To study the effects of contusion and exhaustive exercise on the expression of degradation-related factors MuRF1 and MAFbx in the skeletal muscle of rats and describe the repair mechanism of skeletal muscle injury. Methods Forty-two male SD rats were randomly divided into 7 groups. The rats in each group were killed at different time points (0h, 24h, 48h) after exhaustive exercise (E0, E24, E48) and contusion (D0, D24, D48), respectively, and in the resting state in control group (C). The right gastrocnemius muscles were resected and divided into two parts, one for the mRNAs of MuRF1 and MAFbx by real-time PCR, and the other for protein measurement by Western blotting. Results Compared with the control group, the MuRF1 mRNA and protein expression of the skeletal muscle in the E0 group was markedly increased (P <0.05) and followed by a downward trend in E24 the E48 groups. On the other hand, MuRF1 mRNA expression of the skeletal muscle in the D24 group was significantly upregulated (P <0.01), then decreased in the D48 group (P <0.01). Meanwhile, compared with the C group, MAFbx mRNA gene expression continued to be upregulated in D24 and D48 (P <0.05), but decreased in E24 and E48 (p<0.01). On the other hand, the NF-κB protein contents of the skeletal muscle in the D0, D24, and D48 groups, as well as in the E48 group, were markedly downregulated (P <0.05), and the one in E48 was also remarkably downregulated (P <0.05). Conclusion NF-κB may negatively regulate the process of protein degradation by the NF-κB / MuRF1 signal pathway. Level of evidence III; Therapeutic studies investigating the results of treatment.
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
