柚皮苷防治骨质疏松症的分子机制.

BACKGROUND: Recent studies have shown that research on naringin anti-osteoporosis mostly stays in in vitro and in vivo experiments. Understanding the mechanism of related signaling pathways and the expression of related proteins and some specific genes is an important way to deeply understand naringin anti-osteoporosis. At present, traditional Chinese medicine has been confirmed to have a significant role in anti-osteoporosis. Naringin is one of the main active ingredients in Rhizoma Drynariae. Its effectiveness and mechanism of action against osteoporosis have been gradually recognized by scholars, and its clinical and basic research has been gradually emphasized. OBJECTIVE: To analyze and summarize the research progress of naringin in anti-osteoporosis in vitro and in vivo, thereby providing some ideas for the next step to study its related mechanism of action. METHODS: The relevant literatures included in CNKI and PubMed database were searched with the Chinese search terms of “naringin, osteoporosis, traditional Chinese medicine compound, pathogenesis, signaling pathway, bone marrow mesenchymal stem cells, osteoblasts, osteoclasts” in Chinese and English, respectively. The corresponding criteria were established according to the research needs, and finally 69 articles were included for review. RESULTS AND CONCLUSION: Naringin blocks the increase in the number of osteoclasts and adipocytes, the decrease in the number of osteocytes and osteocalcin (+) cells induced by fructose-rich diet, and promotes the secretion of Sema3A from osteoblasts and osteocytes, thereby enhancing local bone formation and inhibiting osteoclast production by activating the Wnt/β-catenin pathway. Naringin is an important way to induce autophagy of osteoblasts, but autophagy-related proteins participate in osteoblast differentiation and bone formation. Lack of autophagy in osteoblasts reduces mineralization and leads to an imbalance in the number of osteoblasts and osteoclasts, which results in bone loss and decreased bone density. The composite scaffold loaded with naringin can be used as a necessary carrier for bone defect repair and has excellent bone repair properties. Naringin can also accelerate the growth of new bone tissue by increasing the local contents of bone morphogenetic protein 2 and vascular endothelial growth factor. Naringin can regulate bone metabolism and inhibit oxidative stress via ERK, PI3K/Akt and Wnt signaling pathways to improve osteoporosis, which can play a good role in preventing and controlling the disease. However, the depth and breadth of the relevant research is insufficient. Based on the mechanism of the current study, we should investigate the specific mechanisms by which naringin regulates different pathways and inter-pathway interactions in the future, which will be beneficial to the multifaceted development of naringin used in the treatment of osteoporosis.. [ABSTRACT FROM AUTHOR]