摘要
目前,糖皮质激素(glucocorticoids,GC)在临床上被广泛应用于抑制炎症反应与免疫系统,然而GC的长期大量应用会引起破骨细胞过度活跃,导致骨质疏松症以及相关骨折,被称为糖皮质激素性骨质疏松症(GIOP)。GIOP属于中医学“骨痿”“骨枯”的范畴,“骨痿”的发病病机与机体阴阳失衡密切相关。细胞自噬作为一种自我保护机制,对维持机体内环境平衡、调节“成骨-破骨”形成的骨稳态至关重要。成骨细胞与破骨细胞介导的骨稳态与中医理论中的阴阳自和理论不谋而合。本文基于GIOP发病的病机“阳有余而阴不足”探讨通过“调节自噬-平衡阴阳”来调控骨稳态,为防治GIOP提供新的思路。
Currently,glucocorticoids(GC)are widely used in clinical practice to suppress inflammatory responses and the immune system.However,the long-term application of large amounts of GC causes overactive osteoclasts,leading to osteoporosis and related fractures.It is known as glucocorticoid osteoporosis(GIOP),which belongs to the category of bone impotence and bone dryness in Chinese medicine.The pathogenesis of bone impotence is closely related to the imbalance of Yin and Yang in the body.As a self-protective mechanism,cellular autophagy is essential for maintaining the balance of the internal environment of the body and for regulating the bone homeostasis formed by osteogenesis and osteolysis.The osteoblast and osteoclast-mediated bone homeostasis coincide with the theory of Yin and Yang self-healing in Chinese medicine.Based on the pathogenesis of GIOP,which is characterized by excess Yang but not enough Yin,this paper discusses the regulation of bone homeostasis by regulating autophagy and balancing Yin and Yang,and provides a new idea for the prevention and treatment of GIOP.
作者
刘宇
沈耿杨
陈弘林
尚奇
任辉
江晓兵
LIU Yu;SHEN Gengyang;CHEN Honglin;SHANG Qi;REN Hui;JIANG Xiaobing(The First School of Clinical Medicine,Guangzhou University of Chinese Medicine,Guangzhou 510405;Lingnan Medical Research Center of Guangzhou University of Chinese Medicine,Guangzhou 510405;The Second Affiliated Hospital of Guangzhou Medical University,Guangzhou 510260,China)
出处
《中国骨质疏松杂志》
CAS
CSCD
北大核心
2024年第5期708-711,共4页
Chinese Journal of Osteoporosis
基金
国家自然科学基金项目(82274542)
广东省教育厅创新团队项目(2021KCXTD017)
广东省自然科学基金项目(2022A1515012062)
广州中医药大学“双一流”与高水平大学学科协同创新团队(2021xk57)。
关键词
阳有余而阴不足
自噬
糖皮质激素性骨质疏松症
破骨分化
excess Yang but not enough Yin
autophagy
glucocorticoid osteoporosis
osteoclastic differentiation