网站首页期刊介绍通知公告编 委 会投稿须知电子期刊广告合作联系我们
最新消息:
基于“阳化气”理论探讨线粒体-炎症通路在原发性痛经中的作用
作者:刘音吟  周惠芳  李瑾 
单位:南京中医药大学附属医院/江苏省中医院 妇科, 江苏 南京 210029
关键词:原发性痛经 阳化气 温阳法 线粒体 炎症通路 
分类号:R271.11;R249
出版年·卷·期(页码):2025·53·第十期(1574-1579)
摘要:

目的:探讨中西医对原发性痛经(PD)病理机制的认识差异,阐明温经止痛方的治疗机制与价值。方法:结合文献研究梳理PD的西医线粒体功能障碍-炎症机制及中医“阳化气”理论下阳气不足致瘀病机,通过实验验证方药对线粒体及炎症通路的调控作用,并辅以临床观察。结果:温经止痛方可改善线粒体能量代谢、抑制炎症通路,缓解子宫缺血缺氧;临床应用能减轻PD疼痛、改善经期延长,调节内分泌、调整异常指标,部分有生育需求患者治疗后成功妊娠。结论:中西医结合从“线粒体-炎症”双维度揭示PD病机,温经止痛方实现标本兼治,为PD治疗(尤其合并生育需求者)提供新思路。

Objective: To explore the differences in the understanding of the pathological mechanism of primary dysmenorrhea(PD) between traditional Chinese medicine(TCM) and Western medicine, and to clarify the therapeutic mechanism and value of Wenjing Zhitong Decoction. Methods: Based on literature research, this study sorted out the Western medicine's “mitochondrial dysfunction-inflammation mechanism” of PD and the TCM pathogenesis of “blood stasis caused by Yang deficiency” under the theory of “Yang-transforming-Qi”. Experiments were conducted to verify the regulatory effects of the decoction on mitochondria and inflammatory pathways, supplemented by clinical observations. Results: Wenjing Zhitong Decoction could improve mitochondrial energy metabolism, inhibit inflammatory pathways, and alleviate uterine ischemia and hypoxia. Clinically, it could reduce PD-related pain, improve prolonged menstrual periods, regulate endocrine function, and correct abnormal indicators. Some patients with fertility needs successfully conceived after treatment. Conclusion: Integrative Chinese and Western medicine reveals the pathogenesis of PD from the “mitochondria-inflammation” dual dimensions. Wenjing Zhitong Decoction achieves the effect of treating both the root cause and symptoms, providing a new idea for PD treatment(especially for patients with fertility needs).

参考文献:

[1] 姚芡芡,蒲树英,罗艳芳.基于数据挖掘的耳穴埋豆治疗原发性痛经选穴规律分析[J].现代医学,2021,49(4):445-448.
[2] ZHAO L,WANG H,SUN Y,et al.Mitochondrial fission promotes NLRP3 inflammasome activation in dysmenorrhea[J].Cell Death Dis,2021,12(1):88.
[3] VERMA P,SINGH A,GUPTA S,et al.TRPV1-mediated peripheral sensitization in primary dysmenorrhea[J].Pain,2021,162(3):907-918.
[4] 周惠芳,谈津婷,刘贝,等.一种具有治疗黄体功能不全性痛经的中药组合物及其制备方法与应用:中国,CN111481650B[P].2021-11-23.
[5] 黄帝内经素问·阴阳应象大论[M].北京:人民卫生出版社,2012:45.
[6] WANG Y,LI Z,ZHANG W,et al.Yang deficiency patterns and mitochondrial bioenergetics:a systems medicine approach[J].Phytomedicine,2021,90:153.
[7] WU T Y,DOYLE C,Ito J,et al.Cold Exposures in Relation to Dysmenorrhea among Asian and White Women[J].Int J Environ Res Public Health,2024,21(1):56.
[8] WANG L,ZHANG H,LI X,et al.Yangqi modulates gonadotropin-releasing hormone signaling in the reproductive axis[J].Front Endocrinol,2019,10:456.
[9] TAN Y,FLYNN W F,ROBSON P,et al.Single-cell analysis of endometriosis reveals a coordinated transcriptional programme driving immunotolerance and angiogenesis across eutopic and ectopic tissues[J].Nat Cell Biol,2022,24(10):1306-1318.
[10] 张介宾.类经[M].北京:人民卫生出版社,1965.
[11] 王清任.医林改错·气血合脉说[M].上海:上海科学技术出版社,2012:上卷.
[12] 黄帝内经素问·至真要大论[M].北京:人民卫生出版社,2012:312.
[13] WU B N,LI C,WANG X,et al.Mitochondrial bioenergetic dysfunction in dysmenorrheic myometrium[J].Hum Reprod,2020,35(5):1153-1164.
[14] DAI Y,LI J,ZHANG H,et al.ROS-induced mitochondrial dysfunction in primary dysmenorrhea[J].Free Radic Biol Med,2019,143:434-445.
[15] AKOUM A,JOLICOEUR C,BOUCHER A.Estradiol amplifies interleukin-1-induced monocyte chemotactic protein-1 expression by ectopic endometrial cells of women with endometriosis[J].J Clin Endocrinol Metab,2000,85(2):738-745.
[16] BERKLEY K J,MCALLISTER S L,ACCIUS B E,et al.Endometriosis-induced vaginal hyperalgesia in the rat:new insights into mechanisms of pain[J].Pain,2006,126(1-3):263-272.
[17] HERZIG S,SHAW R J.AMPK:guardian of metabolism and mitochondrial homeostasis[J].Nat Rev Mol Cell Biol,2018,19(2):121-135.
[18] 彭鑫,樊攀,吴小涛,等.线粒体形态改变及pink1/parkin通路参与线粒体自噬的研究进展[J].现代医学,2019,47(4):483-487.
[19] LI J,CHEN S,WANG H,et al.Mitochondrial dysfunction in uterine smooth muscle cells correlates with dysmenorrhea severity[J].Cell Mol Life Sci,2020,77(15):2985-2998.
[20] XU R,ZHOU Y,SUN K,et al.AMPK/mTOR signaling mediates energy metabolism imbalance in primary dysmenorrhea models[J].J Transl Med,2019,17(1):1-14.
[21] GAO L,WANG X,HUANG F,et al.ROS accumulation and NLRP3 inflammasome activation in endometriosis-related pain[J].Redox Biol,2021,46:102-104.
[22] LIU T,ZHAO M,ZHANG C,et al.Mitochondrial calcium uniporter regulates uterine contractility through calcium cycling[J].FASEB J,2022,36(3):e22187.
[23] ZHANG W,LI Y,CHEN Z,et al.Yang deficiency promotes NLRP3 inflammasome activation via metabolic reprogramming in endometriosis[J].Front Immunol,2021,12:731892.
[24] CHEN H,DENG Y,WANG S,et al.SIRT1/NF-kB crosstalk mediates Yangqi deficiency-induced inflammatory microenvironment in dysmenorrhea[J].Aging Dis,2020,11(5):1184-1196.
[25] 周惠芳,任青玲,陈赟,等.温经止痛方调控MAPK/ERK通路改善痛经的机制研究[J].中国中药杂志,2022,47(15):4093-4100.
[26] KEKE S W,ZHU W,LAN Z H,et al.Cinnamaldehyde regulates mitochondrial quality against hydrogen peroxide induced apoptosis in mouse lung mesenchymal stem cells via the PINK1/Parkin signaling pathway[J].PeerJ,2022,10:e14045.
[27] LÓPEZ-OTÍN C,BLASCO M A,Partridge L,et al.Hallmarksof aging:an expanding universe[J].Cell,2023,186(2):243-278.
[28] 蔡琳,易小波,袁利邦,等.丹参酮ⅡA通过NLRP3炎症体信号通路对小胶质细胞糖氧剥夺/再灌注损伤的保护作用[J].四川大学学报(医学版),2016,47(5):660-664.
[29] 王伟,戴敏,徐忠东.丹皮酚对脂多糖/三磷酸腺苷诱导的小胶质细胞NLRP3炎症小体激活的影响[J].中国药理学通报,2014,30(5):652-656.

服务与反馈:
文章下载】【发表评论】【查看评论】【加入收藏
提示:您还未登录,请登录!点此登录
您是第 1008139 位访问者


 ©《现代医学》编辑部
联系电话:025-83272481;83272479
电子邮件: xdyx@pub.seu.edu.cn

本系统由北京博渊星辰网络科技有限公司设计开发 技术支持电话:010-63361626

苏ICP备09058541