麦冬在肺纤维化疾病中的作用及机制进展
The Role and Mechanism of Ophiopogon japonicus in Pulmonary Fibrosis Disease
DOI: 10.12677/acm.2025.151240, PDF,    科研立项经费支持
作者: 苏雨晨:成都中医药大学临床医学院,四川 成都;邹雨彤:成都中医药大学附属医院内分泌科,四川 成都;朱万婷:德阳开放大学教学教务处,四川 德阳;林 静:德阳开放大学招生就业处,四川 德阳;柳丽娟:德阳开放大学家庭教育指导中心,四川 德阳
关键词: 麦冬肺纤维化麦冬皂苷D麦冬多糖麦冬甲基黄烷酮AOphiopogon japonicus Pulmonary Fibrosis Ophiopogon Saponin D Ophiopogon Polysaccharides Ophiopogon Methyl Ketone A
摘要: 肺纤维化是多种原因导致的,以细胞外基质过度分泌,导致肺组织结构破坏,形成异常瘢痕组织的慢性间质性肺疾病。目前肺纤维化尚缺少特效治疗药物,开发有效的药物仍是迫切需要解决的一大难题。麦冬是养阴润肺常用药,是治疗肺痿的代表性中药,其药理研究显示具有良好的抗肺纤维化作用,但具体作用机制尚缺乏总结。因此本文对麦冬主要活性成分的药理作用进行归纳,梳理麦冬的主要作用,再对其发挥抗肺纤维化的活性成分进行重点探讨。同时总结了部分以麦冬为主要组成的方剂在肺纤维化中的作用机制,为中西医结合治疗肺纤维化提供思路。
Abstract: Pulmonary fibrosis is a chronic interstitial lung disease caused by multiple factors, including excessive secretion of extracellular matrix, which leads to structural damage of lung tissue and the formation of abnormal scar tissue. At present, there is a lack of specific therapeutic drugs for pulmonary fibrosis, and the development of effective drugs is still an urgent challenge that needs to be addressed. Ophiopogon japonicus is a commonly used medicine for nourishing yin and moistening the lungs, and is a representative traditional Chinese medicine for treating pulmonary dysfunction. Its pharmacological research has shown good anti pulmonary fibrosis effects, but the specific mechanism of action is still lacking in summary. Therefore, this article summarizes the pharmacological effects of the main active ingredients in Ophiopogon japonicus, sorts out the main functions of Ophiopogon japonicus, and then focuses on exploring its active ingredients that exert anti pulmonary fibrosis effects. At the same time, the mechanism of action of some prescriptions mainly composed of Ophiopogon japonicus in pulmonary fibrosis was summarized, providing ideas for the combination of traditional Chinese and Western medicine in the treatment of pulmonary fibrosis.
文章引用:苏雨晨, 邹雨彤, 朱万婷, 林静, 柳丽娟. 麦冬在肺纤维化疾病中的作用及机制进展[J]. 临床医学进展, 2025, 15(1): 1800-1806. https://doi.org/10.12677/acm.2025.151240

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