Article(id=1315688510493938286, tenantId=1146029695717560320, journalId=1315121837170065538, issueId=1315688435411694395, articleNumber=null, orderNo=null, doi=10.16368/j.issn.1674-8999.2025.12.405, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1750089600000, receivedDateStr=2025-06-17, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1791614185211, onlineDateStr=2026-10-10, pubDate=1765296000000, pubDateStr=2025-12-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1791614185211, onlineIssueDateStr=2026-10-10, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1791614185211, creator=13701087609, updateTime=1791614185211, updator=13701087609, issue=Issue{id=1315688435411694395, tenantId=1146029695717560320, journalId=1315121837170065538, year='2025', volume='40', issue='12', pageStart='2487', pageEnd='2712', issueExtLink='null', onlineDate='null', pubDate='1765296000000', pubDateStr='2025-12-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1791614167309, creator='13701087609', updateTime=1791616084449, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1315696476567744680, tenantId=1146029695717560320, journalId=1315121837170065538, issueId=1315688435411694395, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1315696476571938985, tenantId=1146029695717560320, journalId=1315121837170065538, issueId=1315688435411694395, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=2588, endPage=2594, ext={EN=ArticleExt(id=1315688510733013615, articleId=1315688510493938286, tenantId=1146029695717560320, journalId=1315121837170065538, language=EN, title=Research Progress of Traditional Chinese Medicine in Treatment of Atherosclerosis, columnId=1315688445339612089, journalTitle=Acta Chinese Medicine, columnName=Commentary, runingTitle=null, highlight=null, articleAbstract=

Atherosclerosis(AS)is fundamentally rooted in Qi deficiency,with phlegm and blood stasis as its key pathological products. The mutual entanglement of phlegm and blood stasis leading to vascular obstruction is its main pathological manifestation.Effective monomers,herbal pairs,and compound prescriptions of traditional Chinese medicine that tonify Qi,resolve phlegm,activate blood,and unblock collaterals can intervene in the progression of AS through mechanisms such as anti-inflammation,antioxidation,regulation of lipid metabolism,inhibition of cell apoptosis,and improvement of vascular endothelial function,demonstrating the significant advantages of traditional Chinese medicine in the prevention and treatment of AS.The method of benefiting Qi,resolving phlegm,and removing stasis serves as a potential strategy for early intervention in AS and plays an important role in preventing complications such as cardiovascular and cerebrovascular diseases.In the future,the methodology and evaluation system for integrating traditional Chinese medicine(TCM)syndromes with animal models should be further improved. By incorporating findings from modern medical research,the mechanisms of″Qi deficiency,Phlegm and blood stasis″should be explored in depth.At the same time,multicenter,large -sample clinical trials should be conducted to uncover the correlation rules between TCMsyndromes and modern medicine,aiming to provide objective evidence and new insights for the early prevention of atherosclerosis,drug development,optimization of TCM diagnostic and treatment standards,and individualized therapy.

, authors=Xiaoxiao FU, Shan CAO, Xiang QI, authorsList=Xiaoxiao FU, Shan CAO, Xiang QI, authorCompany=null, correspAuthors=Shan CAO, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1315688511131472496, articleId=1315688510493938286, tenantId=1146029695717560320, journalId=1315121837170065538, language=CN, title=中医药治疗动脉粥样硬化研究进展, columnId=1315688445511578555, journalTitle=中医学报, columnName=述评, runingTitle=null, highlight=null, articleAbstract=

动脉粥样硬化(atherosclerosis,AS)以气虚为本,痰、瘀为其关键病理产物,痰瘀互结致血脉瘀阻为其主要病理表现。补气、化痰、活血、通络类中药有效单体、药对配伍及复方均可通过抗炎、抗氧化、调节脂代谢、抑制细胞凋亡及改善血管内皮功能等机制干预AS进展,显示出中医药在防治AS方面的显著优势。益气化痰祛瘀法作为早期干预AS的潜在策略,在预防心脑血管疾病等并发症方面具有重要作用。未来应进一步完善中医病证结合动物模型的构建方法与评价体系,结合现代医学研究成果,深入阐释“气虚痰瘀”的机制;同时开展多中心、大样本临床试验,发掘中医证候与现代医学之间的关联规律,以期为AS的早期预防、药物研发、中医诊疗标准体系优化及个体化治疗提供客观依据与新思路。

, authors=付晓霄, 曹珊, 祁祥, authorsList=付晓霄, 曹珊, 祁祥, authorCompany=null, correspAuthors=曹珊, authorNote=

付晓霄(1999 -),女,河南郑州人,硕士研究生,研究方向:方剂配伍规律与作用机制研究。

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曹珊(1978 -),女,北京人,教授,博士研究生导师,研究方向:方剂配伍规律与作用机制研究。E-mail:
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付晓霄(1999 -),女,河南郑州人,硕士研究生,研究方向:方剂配伍规律与作用机制研究。

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付晓霄(1999 -),女,河南郑州人,硕士研究生,研究方向:方剂配伍规律与作用机制研究。

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中医药治疗动脉粥样硬化研究进展
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付晓霄 , 曹珊 , 祁祥
中医学报 | 述评 2025,40(12): 2588-2594
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中医药治疗动脉粥样硬化研究进展
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付晓霄, 曹珊 , 祁祥
作者信息
  • 河南中医药大学,河南 郑州 450046
通讯作者:
曹珊(1978 -),女,北京人,教授,博士研究生导师,研究方向:方剂配伍规律与作用机制研究。E-mail:
作者简介:

付晓霄(1999 -),女,河南郑州人,硕士研究生,研究方向:方剂配伍规律与作用机制研究。

Research Progress of Traditional Chinese Medicine in Treatment of Atherosclerosis
Xiaoxiao FU, Shan CAO , Xiang QI
Affiliations
  • Henan University of Chinese Medicine, Zhengzhou Henan China 450046
出版时间: 2025-12-10 doi: 10.16368/j.issn.1674-8999.2025.12.405
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动脉粥样硬化(atherosclerosis,AS)以气虚为本,痰、瘀为其关键病理产物,痰瘀互结致血脉瘀阻为其主要病理表现。补气、化痰、活血、通络类中药有效单体、药对配伍及复方均可通过抗炎、抗氧化、调节脂代谢、抑制细胞凋亡及改善血管内皮功能等机制干预AS进展,显示出中医药在防治AS方面的显著优势。益气化痰祛瘀法作为早期干预AS的潜在策略,在预防心脑血管疾病等并发症方面具有重要作用。未来应进一步完善中医病证结合动物模型的构建方法与评价体系,结合现代医学研究成果,深入阐释“气虚痰瘀”的机制;同时开展多中心、大样本临床试验,发掘中医证候与现代医学之间的关联规律,以期为AS的早期预防、药物研发、中医诊疗标准体系优化及个体化治疗提供客观依据与新思路。

动脉粥样硬化  /  气虚  /  血瘀  /  痰浊  /  “气虚痰瘀”  /  痰瘀互结  /  血脉瘀阻  /  中医药

Atherosclerosis(AS)is fundamentally rooted in Qi deficiency,with phlegm and blood stasis as its key pathological products. The mutual entanglement of phlegm and blood stasis leading to vascular obstruction is its main pathological manifestation.Effective monomers,herbal pairs,and compound prescriptions of traditional Chinese medicine that tonify Qi,resolve phlegm,activate blood,and unblock collaterals can intervene in the progression of AS through mechanisms such as anti-inflammation,antioxidation,regulation of lipid metabolism,inhibition of cell apoptosis,and improvement of vascular endothelial function,demonstrating the significant advantages of traditional Chinese medicine in the prevention and treatment of AS.The method of benefiting Qi,resolving phlegm,and removing stasis serves as a potential strategy for early intervention in AS and plays an important role in preventing complications such as cardiovascular and cerebrovascular diseases.In the future,the methodology and evaluation system for integrating traditional Chinese medicine(TCM)syndromes with animal models should be further improved. By incorporating findings from modern medical research,the mechanisms of″Qi deficiency,Phlegm and blood stasis″should be explored in depth.At the same time,multicenter,large -sample clinical trials should be conducted to uncover the correlation rules between TCMsyndromes and modern medicine,aiming to provide objective evidence and new insights for the early prevention of atherosclerosis,drug development,optimization of TCM diagnostic and treatment standards,and individualized therapy.

atherosclerosis  /  Qi deficiency  /  blood stasis  /  Phlegm-Dampness  /  ″Qi deficiency,Phlegm and blood stasis″  /  mutual entanglement of phlegm and blood stasis  /  vascular obstruction  /  traditional Chinese medicine
付晓霄, 曹珊, 祁祥. 中医药治疗动脉粥样硬化研究进展. 中医学报, 2025 , 40 (12) : 2588 -2594 . DOI: 10.16368/j.issn.1674-8999.2025.12.405
Xiaoxiao FU, Shan CAO, Xiang QI. Research Progress of Traditional Chinese Medicine in Treatment of Atherosclerosis[J]. Acta Chinese Medicine, 2025 , 40 (12) : 2588 -2594 . DOI: 10.16368/j.issn.1674-8999.2025.12.405
动脉粥样硬化(atherosclerosis,AS)是心脑血管疾病的核心病理基础,其发生与脂质代谢失衡及异常的炎症反应引起动脉粥样硬化斑块的形成密切相关[1]。据世界卫生组织报道,2019年全球有1 790万人死于心血管疾病,占全球死亡总人数的32%,是导致死亡的主要原因[2]。全球疾病负担2019年研究结果显示,中风是全球第二大死亡原因,占总死亡人数的11.6%[3]。在我国,心血管病患病率持续上升,2021年分别占我国农村、城市死因的48.98%和47.35%,占我国城乡居民死亡原因的首位,而脑血管病死亡率位列我国城乡居民全死因的第三、二位[4]。AS作为一种进展缓慢的疾病,主要发生在老年群体中,其病变特征在于脂质沉积、炎性细胞浸润、平滑肌细胞和坏死细胞碎片的累积和转化。高胆固醇血症、高血压、糖尿病和吸烟等危险因素均参与AS的发病机制[5]。当前,AS常规药物治疗存在严重不良反应,且介入术后新生动脉粥样硬化也已成为关键并发症及治疗瓶颈[6-7]。
中医学无“动脉粥样硬化”的确切病名,但因本病病位在脉管,故多将其归属于“脉痹”范畴,也可根据病因病机、证候等,将其归为“痰浊”“眩晕”“中风”“胸痹”等范畴。中医强调整体观念与辨证论治,通过调整人体整体气机,祛邪气,除痰瘀等病理产物,以达到气血通和、阴阳互调的状态。中医认为本病的基本病机为本虚标实,因虚致邪,标实多与“痰”“瘀”等有关。中药具有多成分、多靶点、多路径治疗的特色及优势,可以健脾益气、活血化痰、通络止痛,从根本上恢复机体阴阳平衡,为临床治疗AS提供参考。
中医学基于“痰”“瘀”“火”“虚”等病理因素,开展了对AS的理论和临床研究[8]。“脉痹”,最初在《素问·痹论》中出现:“风寒湿三气杂至,合而为痹也……以夏遇此者为脉痹。”“痹在于脉则血凝而不流”为其特征。中医认为,AS斑块的病理变化以脾肾气虚为主,并有瘀、毒、痰相互作用[9-10]。中医药对AS斑块的理论和临床研究已有较多报道,气虚、痰浊、血瘀理论受到广泛关注。多数学者认为,痰浊、血瘀互阻于血脉,为发病之标;脏腑之气亏虚致功能失调为本病之本,可累及心、肝、脾、肾诸脏,本虚标实相兼,互为影响,令病势缠绵,病程持续进展[11]。崔应民教授认为气为百病之恶,气虚、气停以致气机不畅、痰瘀绞结,日久伏络是动脉粥样硬化形成的始动因素,痰、瘀、毒既为发病因素,又是病理产物与再发病机[12]。李娜等[13]总结赵凯教授临床经验,认为虚致邪气丛生,形成痰、瘀致气血不通、脉络瘀阻、脉塞斑结为AS病机。纵观古今对脉痹病因病机的认识可以得出,本病的基本病机为本虚标实,因虚致邪,标实多与“痰”“瘀”等有关。
气为血之帅,气行则血行,气血流行正常,脉络则畅达无滞,正如朱震亨《丹溪心法》中记载“气血冲和,万病不生。”气虚在先天责之于肾,在后天责之于脾肺。先天禀赋不足、年老肾气衰退,推动血液运行不利,导致血停瘀滞于脉。如《医林改错》曰:“元气既虚……血管无气,必停留而瘀。”肺为气之本,清气乃宗气之源。若清气摄入不足,则宗气化生减少,久之肺纳气无力,影响宗气“贯心脉”的功能。脾胃既为气血生化之源,又为气机升降之枢,脾胃健运,则气机升降有常[14]。《证治汇补》有言:“脾虚不运清浊,停滞津液而痰生。”《灵枢·本脏》强调:“脾脆则善病消瘅易伤。”《圣济总录·消渴统论》亦载:“肥美之过,积为脾痰。”脾主升清,使精微物质散布全身,阳气得以升发,若过食肥甘,脾气虚弱,则不能升清降浊,运化痰湿,而后产生痰瘀,胶结于脉壁,形成斑块[15]。综上可知,年老、吸烟、高糖高脂饮食均与AS密切相关。王永炎院士结合多年诊治经验和临床实践,提出“虚气留滞”理论[16]。研究发现,气虚质是颈动脉粥样硬化(carotid atherosclerosis,CAS)的高发体质类型之一,年龄和阳虚质是两大独立危险因素[17]。亦有研究发现,原发性高血压合并CAS患者的中医证型中,气血两虚证斑块面积最大[18]。多项研究表明,气虚血瘀型AS能从促进脂质过氧化、升高血清胱抑素C值等途径干预AS的发生发展[19-20]。线粒体是为人体细胞提供能量的场所,是细胞的“能量工厂”,与脾主升清功能相似,因此线粒体功能障碍可视为“脾不升清”的重要病理体现[21]。总而言之,脏腑气机升降失序,阴阳失调,正气损伤,是AS发病的基础。
痰浊是本病的重要病理因素,“百病多有夹痰者”,痰浊病机贯穿AS始终。张闰蕾团队[22]提出“脉生痰核”理论,认为AS斑块的形成和症状特征与痰核流注相符,属于中医“痰核”范畴。血液的正常运行“上下贯通,如环无端”,全赖气为其基本动力,若阳气不足,推动无力,终将引发瘀血的病理状态。刘继东等[23]用“痰浊-痰瘀-痰结”总结了痰瘀交互的不同状态,根据AS发展的不同阶段,提出其内在病机是脾失健运、痰瘀互结。李兆钰等[24]基于丁书文教授“心系疾病热毒论”认为,AS斑块的浓、黏、凝、聚状态与痰瘀互结相契合,其形成与脂代谢紊乱、内皮功能受损及免疫炎症失衡等病理过程密切相关,可归结为痰瘀阻滞,久而化热成毒,损伤脉络,终致痰、瘀、毒三者相互交织的复杂病机。因此,痰瘀同治为治疗AS的重要原则。陈洁等[25]建立了AS痰瘀互结病证结合大鼠模型,采用高脂饮食喂养,予腹腔注射维生素D3,联合颈动脉球囊损伤,使大鼠出现体胖、精神不振、反应迟缓、舌质暗红、舌苔白等痰瘀互结证表现。姜作民[26]在胸痹心痛患者研究中发现,颈动脉Crouse积分为预测和评价动脉粥样硬化和冠脉狭窄程度的理想指标,且胸痹心痛痰瘀证素与CAS具有一定的相关性,血瘀组和痰瘀互结组的颈动脉Crouse积分更高。另有研究指出,CAS患者血清中脂蛋白相关磷脂酶A2(lipoprotein -associated phospholipase A2,Lp -PLA2)、超敏C -反应蛋白(hypersensitive C-reactive protein,hs-CRP)水平与气滞血瘀证密切相关,而低密度脂蛋白胆固醇(low-density lipoprotein cholesterol,LDL-C)、纤维蛋白原(fibrinogen,FIB)水平升高与痰瘀互结证密切相关[27]。由此可知,痰瘀互结是AS形成的关键环节。
脉为奇恒之腑,为血之府也。《灵枢·本脏》曰:“经脉者,所以行血气而营阴阳,濡筋骨,利关节者也。”脉为气血运行之通道,是气血精微输布之枢纽。《黄帝内经》曰:“血脉和利,精神乃居。”血脉瘀阻是以正气亏虚为基,由痰浊、瘀血等病理产物损伤成积所致,中医界有多种理论阐释这一病理表现。王雨涵等[28]基于AS病位特点,提出“脉损”学说,认为“浊逆则损脉,营卫不调则脉道自损”,与西医学的“内皮细胞机械调节”概念不谋而合。陈纪烨等[29]提出“血脉微癥”理论,是以陈可冀院士团队总结的“瘀毒”理论为基础,结合AS斑块的现代微观病理表现及演变规律,认为癥积内生是AS斑块的主要病理表征,表现为病变部位平滑肌细胞的异常增殖、钙盐沉积、胆固醇结晶以及坏死核心等微观结构变化。根据叶天士“久病入络”的观点,许多学者探讨了络脉与AS的关系。张春芹等[30]基于络病学说认为,络道亢变、络道绌急、络久成积是AS进展的重要因素。佟晓雪等[31]基于“正虚络瘀”理论,认为正虚为本,络瘀为标,气血阴阳不足,导致血液运行不畅,血瘀于心,表现为心血瘀阻,络脉不通而痛。李红蓉等[32]认为脉络瘀阻是由功能性病变发展为器质性损伤的重要病程阶段,络息成积是脉络瘀阻的继发性病理改变。靳宏光等[33]从“伏邪”角度指出伏痰、伏瘀始终存在于AS斑块的发生发展过程中,在临床期(动脉粥样斑块期)痰瘀伏络,迁延不愈,壅堵脉络,正不胜邪,触动而发,在心则为胸痹心痛,甚则为真心痛,在脑则可发为中风等疾病。据此可见,血脉瘀阻是AS基本的病理表现。
综上,气虚、痰浊、血瘀是AS形成的基本病机,气虚为本,痰浊、瘀血为标。正虚则邪犯,阴聚则成形,故多数器质性病变疾病,包括血管内脂质积累且有斑块形成的AS在内,均可概括为虚实夹杂的阴阳失衡,致使本病迁延难愈,不断发展,易变生他病。
AS是本虚标实证,因虚致邪,故其治疗应补虚治本,兼除标实。临证可以“气虚痰瘀”理论为指导,以补气为主,化痰活血通络为辅,随证加减治疗AS。中医药可通过单味药、对药、角药、复方等多层次治疗动脉粥样硬化相关疾病,具有多成分、多靶点、多路径的特色和优势。
补气药人参和西洋参的有效成分中均有人参皂苷。药理研究表明,人参皂苷可保护心脑血管,提高机体抗氧化能力,防止血管内皮产生过氧化损伤[34]。人参皂苷Rc(ginsenoside rc,GRc)能显著调节AS小鼠肠道菌群的结构组成[35]。有研究发现,人参皂苷Rd(ginsenoside rd,GRd)能通过抑制炎症反应、氧化应激及核转录因子-κB(nuclear factor kappa-B,NF-κB)信号通路,从而有效抑制AS斑块形成[36]。研究表明,人参皂苷Rb1(ginsenoside Rb1,GRb1)可以通过调控细胞自噬、细胞凋亡防治AS[37]。任丽等[38]发现,GRb1能激活羟甲基戊二酰辅酶A还原酶降解蛋白1(hydroxymethylglutaryl -CoA reductase degradation protein 1,HRD1)通路,抑制氧化应激,进而减少内皮细胞凋亡,发挥抗AS作用。化瘀止血药三七的主要活性成分三七皂苷R1(notoginsenoside R1)具有抗炎、抗凋亡作用,能够减轻氧化应激反应、保护线粒体功能[39]。三七皂苷R1不仅能调控细胞自噬、影响巨噬细胞表型转化改善AS,还能够通过抑制铁死亡减少脂质过氧化,从而改善脂代谢紊乱,抑制动脉粥样斑块形成[40]。另外,活血药丹参活性成分丹参酮ⅡA、活血药姜黄成分姜黄素、补气药黄芪中的黄芪甲苷、解表药柴胡成分柴胡皂苷等均能通过抑制铁死亡发挥防治AS的作用[41]。活血药川芎中的阿魏酸能抑制巨噬细胞的泡沫化,具有抗炎和抗氧化活性作用,还能调节肠道菌群[42]。活血药银杏叶提取物因具有抗氧化、减轻炎症反应、保护内皮细胞、抑制血小板活化、扩张血管以及调节代谢等作用,被广泛运用于治疗心血管疾病[43]。中药沙棘可止咳祛痰、活血散瘀,其主要成分沙棘黄酮能有效减少AS大鼠主动脉内膜脂质沉积,还可调节T淋巴细胞亚群分布,降低细胞信号转导分子3(SMAD family member 3,Smad3)蛋白表达,进而抑制炎症反应,保护血管,预防AS的发生[44]。简而言之,中药活性成分药理作用多样,能从不同途径阐述、分析其治疗AS的机制。
有研究显示,补气药对黄芪-党参能够通过调控肿瘤蛋白p53因子促进AS模型细胞增殖,抑制其凋亡,为临床治疗AS提供了理论基础[45]。任雯庆等[46]研究发现,活血药对丹参-川芎可通过激活磷脂酰肌醇3 -激酶(phosphatidylinositol 3 -kinase,PI3K)/蛋白激酶B(protein kinase B,AKT)信号通路改善血管细胞生长分化,调节血管及血管内皮细胞生理功能,减少冠心病相关症状发生。研究表明,泽泻、白术配伍可补气利水,抑制血管平滑肌细胞(vascular smooth muscle cells,VSMCs)的增殖和表型转化,亦可通过沉默信息调节因子1(silent information regulator 1,SIRT1)-肝X受体α(liver X receptor α,LXRα)-三磷酸腺苷结合盒转运蛋白A1(Adenosine triphosphate -binding cassette transporterA1,ABCA1)/B类1型清道夫受体(scavenger receptor class B type 1,SR-B1)通路促进胆固醇逆转运,减轻肝脏内脂质沉积,改善炎症反应,抑制血管壁增厚和血管狭窄,从而发挥抗AS作用[47-48]。乔羽等[49]通过动物实验得出结论,补气活血药对人参-川芎能够促进白色脂肪棕色化,进而降低慢性间歇性低氧复合肥胖胰岛素抵抗诱导的AS小鼠血脂、血糖水平,发挥抗AS的作用。纪凌云等[50]发现,清热药对黄芩-黄连治疗AS主要是通过介导Toll样受体4(Toll -like receptor 4,TLR4)/髓样分化因子88(myeloid differentiation primary response gene 88,MyD88)/NF-κB信号通路,降低巨噬细胞焦亡水平,发挥抗AS作用。鲍友利等[51]研究表示,化痰散结药对瓜蒌-薤白能通过诱导细胞自噬,抑制核苷酸结合寡聚化结构域样受体蛋白3(NOD-like receptor protein 3,NLRP3)炎症小体的活化,从而减少炎症因子释放抑制巨噬细胞炎症反应。瓜蒌-薤白药对也可能通过抑制p38丝裂原活化蛋白激酶(p38 mitogen activated protein kinase,p38 MAPK)信号通路发挥降脂、抗炎作用,进而实现抗AS效应[52]。此外,化瘀止血药三七也可与补益药、止血活血药、清热药等组成药对,通过中药化学成分间的协同、拮抗或转化等复杂相互作用,实现增效减毒的治疗目的[53]。
角药组合既可独立成方,亦可配伍于复方之中,作为方剂的核心或辅助部分,通过药物间的协同作用,发挥增效减毒之效[54-55]。在治疗心血管疾病方面,角药也具有重要价值。王建云等[56]研究发现“人参-大黄-瓜蒌”配伍可降低血脂上升水平,进而延缓AS进程。三者以人参“扶正培本”为基,大黄“泻浊逐瘀”为用,瓜蒌“化痰通络”为助,形成补虚不滞邪、攻邪不伤正的动态平衡。周蒙蒙[57]对程丑夫教授治疗CAS遣方规律研究发现,其常用角药有十余种,其中“法半夏-甘草-全蝎”配伍以化痰通络止痛为主,兼以补虚。法半夏辛温性燥,主入脾胃,善祛痰湿之邪;甘草补中气、调诸药,能缓和半夏的燥烈和全蝎的毒性;而全蝎辛平通窜、引药入络,能搜剔经络深伏之顽痰瘀毒,改善血管内皮功能障碍,促进局部痰瘀消散。玄参滋阴软化痰结,当归破除血瘀,与甘草协同改善AS“痰瘀互结-脉道狭窄”的核心环节。李洪峥[58]归纳了王阶教授辨治冠心病慢性冠脉综合征的用药规律,“党参-黄芪-肉苁蓉”是其临床常用角药组合。肉苁蓉温肾阳以助血行,黄芪补气以行血,党参、黄芪补气健运,恢复脾肾气化功能,三药合用脾肺肾同补,改善虚损致瘀的结果,且补而不滞,寓通于中,有效避免痰瘀再生。李雪苓教授善治高血压病,“牡丹皮-山药-泽泻”是其常用角药之一,能够清热化瘀、健脾利湿祛浊,是李老多年临床经验与学术积累提炼而成,运用灵活,效果显著[59]。王庆国教授临床上也善用对药、角药以达增强药效之目的,如痰浊壅阻甚者,常用“瓜蒌-薤白-半夏”祛痰化浊、宽胸理气、通阳散结[60]。总而言之,“角药、对药”是临床有效的配伍方式,药味虽少,据证灵活选用,在与治主症病机之方相合过程中,常可获得佳效。
易斯祺[61]研究发现参七脉心通胶囊对气虚血瘀型AS有显著疗效,且抗AS作用可能是通过影响TLR9通路、减少下游信号因子表达进而减少炎症因子的生成实现的,提示TLR9通路可能是AS的潜在治疗靶点。杜高乐[62]研究结果表明,健脾祛痰方可以调节脾虚痰浊AS小鼠主动脉斑块内巨噬细胞极化,减轻炎症对血管的损伤,对AS的发生发展有较好的抑制作用。秦楚峰[63]实验显示健脾通脉方能够通过介导核因子κB抑制物激酶(IκB kinase,IKK)/人核因子κB抑制蛋白α(inhibitor of nuclear factor kappa-B alpha,IKBα)/NF-κB信号通路早期干预AS的进展,并抑制VSMC的增殖、迁移及侵袭,调节其表型转化。李静等[64]研究表明,中药千金黄连丸提取物通过干扰AS大鼠泡沫细胞的形成、调控血脂水平抗AS。冯君等[65]研究表明,降脂消斑片可抑制调控细胞凋亡的天冬氨酸特异的半胱氨酸蛋白酶-8(cysteine-aspartic acid protease-8,Caspase-8)表达及炎症因子释放,这可能是其干预斑块形成的机制。李国铭等[66]将150例脑梗死伴CAS患者分为两组,西药组服用阿托伐他汀,中药组加用益气活血化痰通络法方药(黄芪、丹参、石菖蒲、当归、川芎、瓜蒌、胆南星、陈皮、半夏、地龙、茯苓、炙甘草),用药90d后发现,中药组有效率、颈动脉斑块面积及血脂水平优于西药组。邓梅珍等[67]观察益气活血散(西洋参、三七、丹参、山楂)治疗CAS斑块的临床效果,发现其能有效缓解CAS斑块患者临床症状,对改善斑块形态、降低血脂及保护血管均具有显著效果。Li等[68]研究发现,清血消脂方(虎杖、大黄、蒲黄、姜黄、泽泻、萆薢、茵陈、白术、石菖蒲、红花)能通过改善脂质代谢、抑制脂质沉积和过度炎症反应,从而调节血脂水平,以利于血管壁内皮功能的恢复。Zhang等[69]发现定心方Ⅳ(黄连、丹参、酸枣仁等)通过LXR-α/固醇调节元件结合蛋白1(sterol regulatory element binding protein 1,SREBP 1)途径调节脂代谢及调节肠道菌群减轻动脉粥样硬化。
从体外实验、体内实验到临床研究均证实中医药治疗AS具有巨大优势,能不拘于一方、一证、一药,辨证施治。细胞、分子等微观角度的研究表明,中医药不仅具有抗炎、抗氧化、降血脂、保护血管的作用,还能通过调控铁死亡、自噬、焦亡、凋亡等途径影响细胞形态、迁移与增殖,进而影响疾病的进展。本文基于“气虚痰瘀”理论,论证了气虚、痰浊、血瘀与AS之间的重要关系。正气不足,导致气血津液运行失常而生痰、瘀等病理产物,并瘀阻于脉内形成斑块损伤脉道。秉承中医治未病思想,益气化痰祛瘀法已成为早期干预AS的潜在防治策略,在预防心脑血管疾病等并发症方面具有重要作用。未来需完善中医病证结合动物模型建立方法与评价体系,结合现代医学研究成果,进一步阐释“气虚痰瘀”在AS发病中的作用机制,同时开展多中心、大样本临床试验,发掘中医证候与现代医学之间的关联规律,以期为AS早期预防、新药研发、完善中医诊疗标准体系以及中医个体化治疗寻求客观依据和新的思路。

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2025年第40卷第12期
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doi: 10.16368/j.issn.1674-8999.2025.12.405
  • 接收时间:2025-06-17
  • 首发时间:2026-10-10
  • 出版时间:2025-12-10
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  • 收稿日期:2025-06-17
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    河南中医药大学,河南 郑州 450046

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曹珊(1978 -),女,北京人,教授,博士研究生导师,研究方向:方剂配伍规律与作用机制研究。E-mail:
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2种不同金属材料的力学参数
科
Family
属数
Number of
genus
种数
Number of
species
占总种数比例
Percentage of
total species (%)
属
Genus
种数
Number of
species
占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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