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Mitigation of inflammatory bowel disease-related osteoporosis by oxyberberine: Insights into the RANKL/NF-κB signaling pathway

文献类型： 外文期刊

作者： Chen, Tingting 1 ; Ai, Gaoxiang 2 ; Liang, Guihong 4 ; Zeng, Lingfeng 3 ; Zhao, Di 4 ; Liu, Jun 5 ; Dou, Yaoxing 3 ;

作者机构： 1.Southern Univ Sci & Technol, Sch Med, Shenzhen, Peoples R China

2.Jiangxi Acad Agr Sci, Inst Anim Husb & Vet Sci, Nanchang, Peoples R China

3.Guangzhou Univ Chinese Med, State Key Lab Tradit Chinese Med Syndrome, Postdoctoral Res Stn, Clin Med Coll 2, Guangzhou, Peoples R China

4.Guangzhou Univ Chinese Med, Guangdong Prov Hosp Chinese Med, Affiliated Hosp 2, Guangzhou, Peoples R China

5.Guangdong Prov Acad Chinese Med Sci, Bone & Joint Res Team Degenerat & Injury, Guangzhou, Peoples R China

6.Guangdong Second Tradit Chinese Med Hosp, Guangdong Prov Engn Technol Res Inst Tradit Chines, Guangzhou, Peoples R China

7.Southern Univ Sci & Technol Hosp, Shenzhen, Peoples R China

8.Guangzhou Univ Chinese Med, Affiliated Hosp 2, 12 Jichang Rd, Guangzhou, Guangdong, Peoples R China

关键词： Oxyberberine; Inflammatory Bowel Disease; Osteoporosis; Osteoclast; RANKL/NF; kappa B pathway

期刊名称：BIOMEDICINE & PHARMACOTHERAPY （ 影响因子：7.5； 五年影响因子：6.8 ）

ISSN： 0753-3322

年卷期： 2024 年 174 卷

页码：

收录情况： SCI

摘要： Inflammatory bowel disease is linked to a higher occurrence of bone loss. Oxyberberine can effectively improve experimental inflammatory bowel disease. However, no study has shown the effect of oxyberberine on inflammatory bowel disease induced bone loss. The present study was performed to investigate the role of oxyberberine in inflammatory bowel disease induced osteoporosis in chronic inflammatory bowel disease mice model. The inflammatory bowel disease mice were orally given two doses of oxyberberine daily. Blood, colon, and bone specimens were collected for biomarker assessments and histological examinations. Bone biomechanical properties and key proteins and genes involved in the receptor activator of nuclear factor kappa-B ligand/nuclear factor kappa-B signaling pathway were evaluated. Additionally, the binding characteristics of oxyberberine and receptor activator of nuclear factor kappa-B ligand were evaluated by in silico simulation. Results indicated that oxyberberine treatment significantly attenuated the macroscopic damage, colonic shortening, and histological injury from the colon. Furthermore, oxyberberine decreased serum inflammatory cytokine levels. The intervention with oxyberberine significantly mitigated the deterioration of bone mass, biomechanical properties, and microstructural parameters. Moreover, the upregulated osteoclast formation factors in model mice were significantly abolished by oxyberberine. In silico simulation results also showed that oxyberberine was firmly bound with target protein. Hence, our findings indicated that oxyberberine had the potential to mitigate inflammatory bowel disease induced inflammation in bone, inhibit osteoclast formation through regulating the receptor activator of nuclear factor kappa-B ligand/nuclear factor kappa-B signaling pathway, and might be a valuable approach in preventing bone loss associated with inflammatory bowel disease.

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