Xu Tianyang, Yang Dong, Liu Kaiyuan, Gao Qiuming, Liu Zhongchen, Li Guodong
Department of Orthopedics, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
Department of General Surgery, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
Front Pharmacol. 2022 May 20;13:816891. doi: 10.3389/fphar.2022.816891. eCollection 2022.
The gut microbiota is associated with osteoarthritis (OA) progression. Miya (MY) is a product made from , a member of gut microbiota. This study was conducted to investigate the effects of MY on OA and its underlying mechanisms. An OA rat model was established, and MY was used to treat the rats for 4 weeks. Knee joint samples from the rats were stained with hematoxylin-eosin, and fecal samples from the OA and OA+MY groups were subjected to 16S rDNA sequencing and metabolomic analysis. The contents of succinate dehydrogenase and muscle glycogen in the tibia muscle were determined, and related genes and proteins were detected using quantitative reverse transcription polymerase chain reaction and western blotting. Hematoxylin and eosin staining showed that treatment with MY alleviated the symptoms of OA. According to the sequencing results, MY significantly increased the Chao1, Shannon, and Pielou evenness values compared to those in the untreated group. At the genus level, the abundances of , , , , , and were higher in the OA group, whereas , , , and were enriched after MY treatment. Metabolomic analysis revealed 395 differentially expressed metabolites. Additionally, MY treatment significantly increased the succinate dehydrogenase and muscle glycogen contents in the muscle caused by OA ( > 0.05). Finally, , , , , , , , and were significantly downregulated in the muscles of OA mice, whereas , , and were upregulated; MY significantly reversed these trends induced by OA. MY may promote the repair of joint damage and protect against OA via the gut-muscle-joint axis.
肠道微生物群与骨关节炎（OA）的进展有关。Miya（MY）是一种由肠道微生物群成员制成的产品。本研究旨在探讨MY对OA的影响及其潜在机制。建立了OA大鼠模型，并用MY对大鼠进行治疗4周。对大鼠的膝关节样本进行苏木精-伊红染色，对OA组和OA+MY组的粪便样本进行16S rDNA测序和代谢组学分析。测定胫骨肌肉中琥珀酸脱氢酶和肌肉糖原的含量，并使用定量逆转录聚合酶链反应和蛋白质印迹法检测相关基因和蛋白质。苏木精和伊红染色显示，MY治疗减轻了OA的症状。根据测序结果，与未治疗组相比，MY显著提高了Chao1、Shannon和Pielou均匀度值。在属水平上，OA组中、、、、、和的丰度较高，而MY治疗后、、、和富集。代谢组学分析揭示了395种差异表达的代谢物。此外，MY治疗显著增加了OA引起的肌肉中琥珀酸脱氢酶和肌肉糖原的含量（>0.05）。最后，、、、、、、、和在OA小鼠肌肉中显著下调，而、、和上调；MY显著逆转了OA诱导的这些趋势。MY可能通过肠-肌肉-关节轴促进关节损伤的修复并预防OA。
