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. 2024 Dec 30;25(1):1081.
doi: 10.1186/s12891-024-08203-5.

The effect of Miya on skeletal muscle changes by regulating gut microbiota in rats with osteoarthritis through AMPK pathway

Sen Wang #  1 , Zhengwei Duan #  1 , Zihua Li  1 , Dong Yang  1 , Hengli Lu  1 , Yiwei Zhang  1 , Yuesong Fu  1 , Yonghao Guan  1 , Guodong Li  1 , Feng Qian  2 , Tianyang Xu  3
Affiliations

The effect of Miya on skeletal muscle changes by regulating gut microbiota in rats with osteoarthritis through AMPK pathway

Sen Wang et al. BMC Musculoskelet Disord. .

Abstract

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.

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.

Conclusion: MY may partially regulate skeletal muscle changes and prevente OA development through the AMPK pathway.

Keywords: AMPK; Gut microbiota; Miya; Osteoarthritis.

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Conflict of interest statement

Declarations. Ethics approval and consent to participate: All animal studies were conducted in compliance with guidelines and regulations. All the animal experiments were approved by the Ethics Committee of Shanghai Tenth People's Hospital, Tongji University School of Medicine. And the study is reported in accordance with the relevant ARRIVE guidelines. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
The histological changes of rats in the different groups observed by hematoxylin–eosin (HE) staining at 40 × , 100 × and 200 × magnification times. The green arrow indicates the surface of the cartilage; the yellow arrow points to cells; the red arrow indicates the tide line; and the blue arrow indicates the absence of cells. The rough triangle represents the nucleus; and the thin arrow represents the cytoplasm. Control: the rats without any treatments; OA: the osteoarthritis (OA) rat model; OA + MY: the OA rats treated with Miya (MY); OA + MY + adenosine 5’-monophosphate-activated protein kinase (AMPK) inhibitor: the OA rats firstly treated with MY, and then treated with BML275 (dorsomorphin, an AMPK inhibitor)
Fig. 2
Fig. 2
Effects of the AMPK inhibitor on the succinate dehydrogenase (SDH) and muscle glycogen (MG) in MY-treated OA. A The contents of SDH in the tibia muscle of different groups. B The contents of MG in the tibia muscle of different groups. * p < 0.05, compared with the OA + MY group
Fig. 3
Fig. 3
Effects of the AMPK inhibitor on the mRNA levels of associated genes in the MY-treated OA using real-time quantitative PCR. The mRNA expression levels of (A) AMPK, (B) PI3K, (C) AKT1, (D) mTOR, (E) p70s6k, (F) Ldh, (G) Lcad, (H) Mcad, (I) Myod, (J) Murf-1, (K) Chrna1, (L) Chrnd in the different groups. * p < 0.05, compared with the OA + MY group
Fig. 4
Fig. 4
Effects of the AMPK inhibitor on the protein levels of the associated proteins in the MY-treated OA by western blot. A The protein bands of all the associated proteins visualized by western blot analysis. The protein expression levels of (B) AMPK, (C) PI3K, (D) Ldh, (E) Lcad, (F) Mcad, (G) Myod, (H) Chrna1, (I) Chrnd in the different groups. * p < 0.05, compared with the OA + MY group
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