摘要
老年性骨质疏松症(SOP)作为一种代谢性骨病,表现为成骨细胞及破骨细胞数量的失衡。铁死亡是一种以铁依赖性脂质过氧化,活性氧堆积为特征的新型细胞死亡类型。近年来,越来越多的研究证实铁死亡的独特生物学特征,例如铁过载、脂质过氧化物积累参与并影响SOP的发生及发展,这与中医学的“浊毒致病”理论相契。“浊毒”阻滞气机、损伤气血阴阳,作为致病因素与病理产物的统一体奠定了SOP的发病基础。本文从“浊毒”理论、铁死亡与SOP三者之间的关系进行论述,探析并拓展SOP的发病机制,为中医药防治SOP提供新思路。
Senile osteoporosis(SOP) as a metabolic bone disease,is characterized by an imbalance in the number of osteoblasts and osteoclasts.Ferroptosis is a new type of cell death characterized by iron-dependent lipid peroxidation and reactive oxygen species accumulation.In recent years,more and more studies have confirmed that the unique biological characteristics of ferroptosis,such as iron overload and lipid peroxides accumulation participating in and affect the occurrence and development of SOP,which is consistent with the theory of“turbid toxicity causing”in traditional Chinese medicine.“Turbid toxicity”blocks qi activity,damages qi,blood,yin,and yang,which lays the foundation for the pathogenesis of SOP as the unity of pathogenic factors and pathological products.This paper discuss the relationship between“turbid toxicity”theory,ferroptosis and SOP,explores and expands the pathogenesis of SOP,and provides new ideas for traditional Chinese medicine prevention and treatment of SOP.
作者
贾洪洋
白蕊
李双蕾
王婷
曾施琪
郑洪香
陈文辉
JIA Hongyang;BAI Rui;LI Shuanglei;WANG Ting;ZENG Shiqi;ZHENG Hongxiang;CHEN Wenhui(Graduate School,Guangxi University of Chinese Medicine,Guangxi Zhuang Autonomous Region,Nanning530001,China;Faculty of Chinese Medicine Science Guangxi University of Chinese Medicine,Guangxi Zhuang Autonomous Region,Nanning530222,China;Department of Endocrinology,the First Affiliated Hospital of Guangxi University of Chinese Medicine,Guangxi Zhuang Autonomous Region,Nanning530023,China)
出处
《中国医药导报》
CAS
2024年第13期172-174,共3页
China Medical Herald
基金
国家自然科学基金地区科学基金项目(82360869)
广西自然科学基金项目(2020GXNSFAA297193)
中国民族医药学会科研项目(2021Z1141-580302)
广西高校中青年教师科研基础能力提升项目(2023KY1743)
广西中医药大学赛恩斯新医药学院校级科研项目(2022MS003)
广西中医药大学研究生教育创新计划项目(YCBXJ2023004、YCSY2022022)。
关键词
老年性骨质疏松症
铁死亡
浊毒
骨代谢
Senile osteoporosis
Ferroptosis
Turbid toxicity
Bone metabolism
