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Qin Yin Department of Orthopedics, Wuxi Ninth People’s Hospital Affiliated to Soochow University, Wuxi, Jiangsu, China

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Jun Gu Department of Orthopedics, Wuxi Ninth People’s Hospital Affiliated to Soochow University, Wuxi, Jiangsu, China

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Pengju Ren Department of Orthopedics, The Shanghai Tenth People’s Hospital of Tongji University, Shanghai, China

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Zhiqiang Guan Department of Dermatology, Xuzhou Municipal Hospital Affiliated to Xuzhou Medical University, Xuzhou, Jiangsu, China

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Yongxiang Wang Department of Orthopedics, Clinical Medical College, Yangzhou University, Yangzhou, China
Department of Orthopedics, Northern Jiangsu People’s Hospital, Yangzhou, China

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Ruijun Bai Department of Orthopedics, Wuxi Ninth People’s Hospital Affiliated to Soochow University, Wuxi, Jiangsu, China

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Yu Liu Department of Orthopedics, Wuxi Ninth People’s Hospital Affiliated to Soochow University, Wuxi, Jiangsu, China

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The role of this study was to evaluate the impact of gut microbiota depletion on the progression of osteoarthritis (OA) and osteoporosis (OP). We conducted an experimental mouse model of OA and OP over an 8-week period. The model involved destabilization of the medial meniscus and bilateral ovariectomy (OVX). To deplete the gut microbiota, we administered a course of antibiotics for 8 weeks. The severity of OA was assessed through micro-CT scanning, X-rays, and immunohistochemical staining. Microbiome analysis was performed using PCR of 16S DNA on fecal samples, and the levels of serum lipopolysaccharide, interleukin 6, tumor necrosis factor-α (TNF-α), osteocalcin, and estrogen were measured using enzyme-linked immunosorbent assay. We found that in comparison to the OVX+OA group, the OVX+OA+ABT group exhibited increased bone mineral density (P < 0.0001), bone volume fraction (P = 0.0051), and trabecular number (P = 0.0023) in the metaphyseal bone. Additionally, cartilage injury and levels of matrix metalloproteinase 13 were reduced in the OVX+OA+ABT group compared to the OVX+OA group. Moreover, the OVX+OA+ABT group demonstrated decreased relative abundance of Bacteroidetes, serum lipopolysaccharide (P = 0.0005), TNF-α (P < 0.0001), CTX-1 (P = 0.0002), and increased expression of bone formation markers. These findings were further supported by correlation network analyses. Depletion of gut microbiota was shown to protect against bone loss and cartilage degradation by modulating the composition of the gut microbiota in osteoporosis and osteoarthritis.

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Jin-Bong Lee Metabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon Republic of Korea
Department of Functional Genomics, University of Science and Technology, Daejeon, Republic of Korea

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Sung-Jin Yoon Immunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea

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Sang-Hyun Lee Biotherapeutics Translational Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea

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Moo-Seung Lee Department of Biomolecular Science, University of Science and Technology, Daejeon, Republic of Korea
Infectious Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea

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Haiyoung Jung Department of Functional Genomics, University of Science and Technology, Daejeon, Republic of Korea
Immunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea

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Tae-Don Kim Department of Functional Genomics, University of Science and Technology, Daejeon, Republic of Korea
Immunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea

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Suk Ran Yoon Department of Functional Genomics, University of Science and Technology, Daejeon, Republic of Korea
Immunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea

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Inpyo Choi Department of Functional Genomics, University of Science and Technology, Daejeon, Republic of Korea
Immunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea

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Ik-Soo Kim Hanwool Life Sciences, Daejeon, Republic of Korea

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Su Wol Chung School of Biological Sciences, College of Natural Sciences, University of Ulsan, Ulsan, Republic of Korea

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Hee Gu Lee Department of Functional Genomics, University of Science and Technology, Daejeon, Republic of Korea
Department of Biomolecular Science, University of Science and Technology, Daejeon, Republic of Korea

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Jeong-Ki Min Biotherapeutics Translational Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea
Department of Biomolecular Science, University of Science and Technology, Daejeon, Republic of Korea

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Young-Jun Park Metabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon Republic of Korea
Immunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea

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Healthy expansion of adipose tissue maintains metabolic homeostasis by storing excess chemical energy in increased fat mass. The STAT5-PPAR gamma pathway reportedly regulates adipocyte differentiation, lipid metabolism and adipogenesis. Ginsenoside Rg3 is one of the diverse groups of steroidal saponins, the major active components of ginseng, which have demonstrated pharmacological properties. In this study, we evaluated the therapeutic effects of ginsenoside Rg3 under pathological conditions in vitro and in vivo. We examined the effects of ginsenoside Rg3 on glucose level, insulin sensitivity and lipogenesis in high-fat diet-fed C57BL/6 mice. Ginsenoside Rg3 was also applied to the pre-adipocyte cell line 3T3-L1 to assess the impact on lipogenesis. Ginsenoside Rg3 reduced epididymal white adipose tissue (eWAT) size and hepatic steatosis, and the amount of triglycerides (TGs) in both eWAT and liver. Similar to the murine model, Rg3-treated 3T3-L1 cells showed a reduction in lipid accumulation and amount of total TGs. Ginsenoside Rg3 regulates the expression of PPAR gamma though STAT5 in vitro and in vivo. According to our results, lipid metabolism-related genes were downregulated in the high-fat mice and 3T3-L1 cell line. Rg3 shows potential for the amelioration of obesity-induced pathology, acting though STAT5-PPAR gamma to facilitate the healthy functioning of adipose tissue. This is the first report of evidence that obesity-induced insulin resistance and lipotoxicity can be treated with ginsenoside Rg3, which acts though the STAT5-PPAR gamma pathway in vivo and in vitro.

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