Background
The study aimed to explore whether Miya (MY), a kind of Clostridium butyricum, regulated osteoarthritis (OA) progression through adenosine 5'-monophosphate-activated protein kinase (AMPK) pathway.
Conclusion
MY may partially regulate skeletal muscle changes and prevente OA development through the AMPK pathway.
Methods
The OA rats were orally given MY daily for 4 weeks and were intramuscularly injected with AMPK inhibitor once a week for 4 weeks. Hematoxylin eosin (HE) staining was used to observe the histological morphology of the knee joint. The levels of succinate dehydrogenase (SDH) and muscle glycogen (MG) in the tibia muscle of rats were detected by the corresponding kits, as well as the expression of related genes/proteins were assessed by real-time quantitative PCR (RT-qPCR) and western blot.
Results
HE staining suggested that MY suppressed the symptoms of OA, which was abolished by AMPK inhibitor. Furthermore, the SDH and MG contents in the OA + MY + AMPK inhibitor group were lower than in the OA + MY group. At last, the levels of AMPK, PI3K, AKT1, Ldh, Myod, Chrna1, and Chrnd were notably decreased after AMPK inhibitor treatment, while the levels of Lcad and Mcad were up-regulated by AMPK inhibitor. Furthermore, their protein expression levels detected by western blot were consistent with those from RT-qPCR.