The American journal of Chinese medicine最新文献

{"title":"A Comprehensive Review on Botany, Ethnopharmacology, Phytochemistry, Biosynthesis, Pharmacology, Toxicity, Quality Control and Metabolomics of Coptidis Rhizome.","authors":"Anlu Liao, Min Han, Shujing Chen, Chuanyuan Gao, Wei Wei, Jin Li, Kunze Du, Yanxu Chang","doi":"10.1142/S0192415X25500648","DOIUrl":"10.1142/S0192415X25500648","url":null,"abstract":"<p><p>Coptidis Rhizome (CR), referred to as Huanglian in Chinese, is the dry rhizome of <i>Coptis chinensis</i> Franch., <i>Coptis deltoidea</i> C.Y. Cheng et Hsiao, or <i>Coptis teeta</i> Wall. This herbal remedy is renowned for its heat-clearing, dampness-drying, and detoxifying properties. In traditional medical applications, it is frequently employed to address disorders such as gastroenteritis, jaundice, eczema, and various other health issues. This article reviews the latest developments in the fields of CR botany, ethnopharmacology, phytochemistry, biosynthesis, pharmacology, pharmacokinetics, toxicology, quality control, and metabolomics. These discoveries enhance the scientific basis for continued research and utilization of CR in medicine. Currently, over 200 compounds from CR, including alkaloids, lignans, phenolic compounds, flavonoids, polysaccharides, volatile oils, and other constituents, have been identified. Among these, alkaloids are the most abundant and represent the primary bioactive components. CR and its active alkaloids display a broad spectrum of pharmacological impacts, which include anti-inflammatory, anticancer, hypoglycemic, and cardiovascular disease treatments. In recent years, the research progress on CR in plant chemistry, pharmacology, and quality control has demonstrated its effectiveness and provided guidance for further research. This review will provide a reference for the development and utilization of CR in the future.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1711-1754"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144762899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis in Endometriosis: Traditional Chinese Medicine Interventions and Mechanistic Insights.","authors":"Dingli Lan, Shuping Huang, Jing Li, Shilang Zhou, Jianli Deng, Shuiyun Qin, Ting Zhou, Fengyun Meng, Weihong Li","doi":"10.1142/S0192415X25500156","DOIUrl":"10.1142/S0192415X25500156","url":null,"abstract":"<p><p>Endometriosis (EMS) is a chronic, estrogen-dependent inflammatory disease affecting 5-10% of women of reproductive age, characterized by the growth of endometrial tissue on the outside of the uterus. The dysregulation of iron metabolism leads to the accumulation of iron ions at the lesion sites, resulting in oxidative stress and pro-inflammatory responses that promote the progression of EMS. The mechanisms underlying ferroptosis in EMS primarily involve iron accumulation, lipid peroxidation, and loss of glutathione peroxidase 4 activity. These mechanisms confer resistance to ferroptosis within the ectopic tissues and facilitate cell survival and proliferation. Traditional Chinese medicine (TCM) has demonstrated therapeutic potential for modulating ferroptosis. Studies have shown that TCM monomers may regulate ferroptosis by modulating iron transport proteins and anti-oxidant defense mechanisms. TCM formulas employ distinct treatment strategies depending on the stage of EMS: in the early stages, they promote ferroptosis to control lesion growth, whereas in the later stages, they inhibit ferroptosis to reduce oxidative stress and inflammation in order to improve reproductive health and slow disease progression. This study provides a new perspective on potential therapeutic strategies for the management of EMS by summarizing the role of ferroptosis in its pathological mechanisms and reviewing findings on the use of TCM in regulating ferroptosis.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"385-408"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143723061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Gastrodia elata</i> Polysaccharide Ameliorates Parkinson's Disease by Enhancing Dopamine Levels, Inhibiting NLRP3 Inflammasome Activation, and Promoting Mitochondrial Autophagy.","authors":"Shidai Li, Ming Li, Yangping Li, Si Liang, Li Ling, Hongjie Wang, Jiguang Guo","doi":"10.1142/S0192415X25500673","DOIUrl":"10.1142/S0192415X25500673","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a progressive neurodegenerative disorder marked by dopaminergic (DA) neuron loss and neuroinflammation. Current therapies fail to halt disease progression, which underscores the need for new treatments. This study investigated the neuroprotective effects and mechanisms of <i>Gastrodia elata</i> polysaccharide (GEP) in MPTP-induced PD mice. GEP was administered for two weeks, and motor function was assessed using behavioral tests. Immunohistochemical and Western Blot analyses evaluated DA neuron survival, microglial activation, and NLRP3 inflammasome components. GEP-medicated serum (GMS) was applied to SH-SY5Y neuroblastoma cells exposed to neuroinflammatory conditions, and metabolomic analysis identified key metabolites. GEP improved motor function, reduced DA neuron loss, and increased tyrosine hydroxylase expression. It suppressed microglial activation, decreased NLRP3 inflammasome components, and lowered pro-inflammatory cytokines (IL-1β, IL-6, TNF-α). GMS reduced ROS levels, enhanced mitochondrial membrane potential, and promoted autophagy in SH-SY5Y cells. Metabolomic analysis revealed elevated dopamine levels in GMS, linked to NLRP3 inflammasome inhibition, and reduced neuroinflammation. GMS also activated the PINK1/Parkin pathway to promote mitochondrial autophagy and prevent apoptosis. GEP alleviates PD symptoms by targeting neuroinflammation, mitochondrial dysfunction, and dopamine regulation, which highlights its potential as a therapeutic candidate. Further research is needed to explore its long-term efficacy and clinical applications.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1813-1844"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144839585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Korean Red Ginseng Marc-Derived Gintonin Improves Alzheimer's Cognitive Dysfunction by Upregulating LPAR1.","authors":"Yujeong Ha, Rami Lee, Seung Ho Jeon, Ji-Hun Kim, Hyo-Sung Jo, Tae Woo Kwon, Sung-Hee Hwang, Jong Kil Lee, Seung-Yeol Nah, Ik-Hyun Cho","doi":"10.1142/S0192415X25500028","DOIUrl":"10.1142/S0192415X25500028","url":null,"abstract":"<p><p>Ginseng is a well-established functional food for brain health. However, its active ingredients have not yet been identified. Gintonin is a promising compound isolated from white/red ginseng. Its lysophosphatidic acid (LPA) is an exogenous G protein-coupled LPA receptor (LPAR) agonist. Korean red ginseng marc (KRGM) is a by-product after KRG extractions. In a previous study, we demonstrated that KRGM-derived gintonin (KRGM-G) contains LPA C[Formula: see text], a major functional component of both white and red ginseng. [Formula: see text] transgenic mice and SH-SY5Y cells were used to determine molecular mechanisms involved in KRGM-G-mediated anti-Alzheimer's disease (AD) effects. KRGM-G improved cognition impairment associated with alleviation of amyloid-β accumulation in the brain (hippocampus and cortex) in [Formula: see text] mice. KRGM-G inhibited activation of inflammatory cells (Iba-1-positive microglia and GFAP-positive astrocyte) and expression of pro-inflammatory mediators (IL-1β, IL-6, iNOS, or NO) in the brains of [Formula: see text] mice, increased the viability of H₂O₂-induced SH-SY5Y cells, and down-regulated the p38 MAPK, NF-κB p65, and STAT3 signaling pathways. KRGM-G also prevented the formation of reactive oxygen species and stimulated the Nrf2-HO-1/4-HNE signaling pathway in the brains of [Formula: see text] mice and SH-SY5Y cells. Interestingly, these positive effects of KRGM-G on AD-related symptoms and immunopathology were associated with up-regulation of LPAR1 in the brains of [Formula: see text] mice. These results suggest that KRGM-G might improve AD-related cognitive dysfunction by stimulating the anti-oxidant pathway (Nrf2) and inhibiting inflammatory pathways (p38/NF-κB/STAT3) through LPAR1.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"17-41"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Puerarin Attenuates Myocardial Ischemia-Reperfusion Damage by Targeting Ferroptosis through 14-3-3η Modulation.","authors":"YaMei Qiao, SongQing Lai, YaRu Wang, FaJia Hu, Yue Liu, FeiXiang Zhai, ZeYu Zhang, Dan Liu, Huang Huang","doi":"10.1142/S0192415X25500570","DOIUrl":"10.1142/S0192415X25500570","url":null,"abstract":"<p><p>Myocardial ischemia-reperfusion (I/R) injury continues to be a significant clinical challenge, and ferroptosis has been identified as a major contributing factor to its development. Puerarin (Pue), an isoflavone derived from <i>Pueraria lobata</i>, has demonstrated promising cardioprotective effects, although the mechanisms involved are not fully elucidated. This study explores Pue's ability to attenuate myocardial I/R damage through the modulation of ferroptosis, specifically focusing on the role of the 14-3-3η protein. Network pharmacology identified 356 potential targets for Pue, with 25 genes overlapping between myocardial I/R injury and ferroptosis pathways. Molecular docking analysis revealed a strong interaction between Pue and 14-3-3η, suggesting a mechanistic link. <i>In vitro</i> studies using H9c2 cardiomyocytes showed that Pue pretreatment significantly improved cell viability and reduced lactate dehydrogenase (LDH) release under conditions of anoxia/reoxygenation (A/R). Pue's inhibition of ferroptosis was evidenced by reduced iron accumulation, decreased malondialdehyde (MDA) levels, lowered reactive oxygen species (ROS), and boosted anti-oxidant defenses. Central to these protective effects was the upregulation of 14-3-3η, and knockdown experiments confirmed its pivotal role in ferroptosis regulation. Furthermore, Pue preserved mitochondrial function by stabilizing mitochondrial membrane potential, limiting mitochondrial permeability transition pore (mPTP) opening, and improving mitochondrial energy metabolism and structural integrity. These activities were all mediated by 14-3-3η. <i>In vivo</i>, Pue administration in a rat I/R model significantly reduced myocardial injury markers and improved cardiac function, and its effects were reversed when 14-3-3η expression was downregulated. This study provides compelling evidence that Pue mitigates myocardial I/R injury by inhibiting ferroptosis through 14-3-3η modulation, and presents a novel therapeutic avenue for cardioprotection.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1501-1520"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective Effects of <i>Paeonia lactiflora</i> Through the Regulation of Gut <i>Dubosiella</i> in an MPTP-Induced Parkinson's Disease Mouse Model.","authors":"Xian Shao, Mengyun Li, Shuai Shi, Tao Wu, Yanxing Zhang, Shitian Guo, Hui Lin, Xuchen Qi","doi":"10.1142/S0192415X25500314","DOIUrl":"https://doi.org/10.1142/S0192415X25500314","url":null,"abstract":"<p><p>Emerging evidence suggests that changes in the composition of the gut microbiota may play an important role in the pathogenesis of Parkinson's disease (PD). <i>Paeonia lactiflora</i> Pall., a traditional Chinese medicinal herb belonging to the genus <i>Paeonia</i>, is commonly used in Chinese medicinal practice for the treatment of PD. However, the specific mechanisms of its action remain poorly understood. This study aimed to further determine the neuroprotective properties of <i>Paeonia lactiflora</i> Pall. water extract (PWE) in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model, and to investigate its potential implications for the pathogenesis of PD. A PD mouse model was established via the intraperitoneal administration of MPTP, followed by the assessment of motor function using behavioral tests. Western blotting and histopathological analysis were used to measure the levels of dopaminergic (DAergic) neurodegeneration-related factors in the midbrain (containing the substantia nigra (SN)) and striatum. 16S rRNA gene sequencing and metabolomic analysis were applied to identify differences in the gut microbiota and metabolites, respectively. Our results indicate that PWE effectively protects against MPTP-induced motor deficits, loss of DAergic neurons, blood-brain barrier (BBB) damage, and neuroinflammation in PD. The protective effects of PWE against PD are mediated through modulation of the gut microbiota, specifically by an increase in the abundance of the genus <i>Dubosiella</i>. In this study, we selected <i>D. newyorkensis</i> as a representative strain of the genus, and determined its therapeutic effects in an MPTP-induced PD mouse model. Our preliminary findings suggest that the neuroprotective effects of <i>D. newyorkensis</i> may be related to the production of serum indoleacetic acid.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"53 3","pages":"833-862"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Pharmacology and Toxicology of Ginkgolic Acids: Secondary Metabolites from <i>Ginkgo biloba</i>.","authors":"Yuting Shao, Yun Chen, Qingyu Zhu, Lingyan Yi, Yifan Ma, Xiangxu Zang, Wenjuan Yao","doi":"10.1142/S0192415X25500077","DOIUrl":"10.1142/S0192415X25500077","url":null,"abstract":"<p><p>Ginkgolic acids (GAs) are distinctive secondary metabolites of <i>Ginkgo biloba</i> (<i>G. biloba</i>) primarily found in its leaves and seeds, with the highest concentration located in the exotesta. GAs are classified as long-chain phenolic compounds, and exhibit structural similarities to lignoceric acid. Their structural diversity arises from variations in the length of side chains and their number of double bonds, resulting in six distinct forms within <i>G. biloba</i> extracts (GBE). Of these, GA (C15:1) is the most prevalent. As inhibitors of SUMOylation, GAs demonstrate significant antitumor activity, and can exert antineoplastic effects through multiple pathways, which positions them as potentially promising therapeutic agents for cancer treatment. Additionally, GAs exhibit notable anti-inflammatory, antibacterial, and antiviral properties, highlighting their multifaceted medicinal potential. Although the pharmacological properties of GAs have been extensively investigated, the associated risks of liver and kidney damage must not be overlooked. GAs can induce significant hepatic damage by promoting cellular apoptosis, oxidative stress, and the disruption of various metabolic processes. Furthermore, a limited number of studies have indicated that GAs may exhibit nephrotoxicity, as well as adverse effects on the skin and nervous system. Due to their recognized toxicity, the concentration of GAs is typically regulated to within 5[Formula: see text]ppm in the standardized <i>G. biloba</i> leaf extract EGb 761. Currently, there is no definitive evidence supporting the mutagenic toxicity of GAs. This review primarily synthesizes recent advancements in understanding the pharmacological and toxicological effects of GAs, along with their underlying mechanisms. It is anticipated that this review will stimulate scholarly discourse and elicit valuable insights.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"147-177"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Pharmacological Effects of Gastrodin and the Progress in the Treatment of Neurological Disorders.","authors":"Han Guo, Dongmei Cheng, Cong Zhang, Fang Xue","doi":"10.1142/S0192415X25500302","DOIUrl":"https://doi.org/10.1142/S0192415X25500302","url":null,"abstract":"<p><p><i>Gastrodia elata</i> Blume, a traditional medicinal herb primarily used in Asian countries such as China, has long been valued for treating headaches, dizziness, spasms, epilepsy, strokes, forgetfulness, and other ailments. Gastrodin, a glycoside analog and major bioactive component of <i>Gastrodia elata Blume</i>, has garnered significant scientific attention owing to its extensive pharmacological effects. It is commonly obtained through plant extraction, chemical synthesis, and biosynthesis. Gastrodin exhibits remarkable modulatory effects on the central nervous system (CNS), with promising applications in epilepsy, neurodegenerative diseases such as Parkinson's disease (PD) and Alzheimer's disease (AD), and affective and cognitive disorders. Furthermore, the pharmacokinetics (PK) of gastrodin has been extensively reviewed. As a small molecule drug, this study focused on its efficiency and molecular mechanisms in treating CNS disorders, aiming to elucidate its interactions with disease targets. This study provides valuable insights for its development and addresses the drawbacks of unclear pharmacological mechanisms in traditional Chinese medicine.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"53 3","pages":"803-831"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Berberine Inhibited SASP-Related Inflammation through RXRα/PPARγ/NEDD4 Pathway in Atherosclerosis.","authors":"Yinghong Zheng, Jiayuan Kou, Xi Gao, Jinxiang Guo, Qian Liu, Huiwen Ren, Tielei Gao, Qianbing Wang, Yajie Zhao, Yuqin Wang, Hong Li, Liming Yang","doi":"10.1142/S0192415X25500107","DOIUrl":"10.1142/S0192415X25500107","url":null,"abstract":"<p><p>The accumulation of aging cells significantly contributes to chronic inflammatory diseases such as atherosclerosis. Human carotid artery single-cell sequencing has shown that large numbers of aging foam cells are present in the plaques of human patients. Berberine (BBR) has been shown to inhibit cell senescence, however, the mechanisms involved in its treatment of atherosclerotic senescence have not yet been determined. Changes in plaque morphology and blood chemistry were observed in ApoE[Formula: see text] mice fed with a high-fat diet before and after BBR treatment. Inflammatory proteins linked to the senescence-associated secretory phenotypes (SASP) were detected in RAW264.7 and peritoneal macrophage-derived foam cells. Smart-seq analysis was used to explore the pathways associated with BBR therapy for atherosclerosis. Finally, the effect of lentivirus-mediated knockdown of RXRα in macrophages in plaques on atherosclerosis treatment with BBR was determined. We found that BBR reduced inflammation linked to SASP in atherosclerosis through the RXRα/PPARγ/NEDD4 signaling pathway. BBR increased GATA4 binding to p62, promoted ubiquitination, and inhibited SASP-associated protein production in RAW264.7 and peritoneal macrophage-derived foam cells. Mechanistically, according to the Smart-seq results, BBR activated RXRα and PPARγ, synergistically increased NEDD4 transcription levels, and promoted ubiquitination-mediated degradation of the GATA4/p62 complex. Additionally, the anti-aging impact of BBR on atherosclerosis was negated when macrophage-specific RXRα was knocked down using lentivirus (pLVCD68-shRNA RXRα) in ApoE[Formula: see text] mice. BBR activated PPARγ through RXRα-PPARγ immune complex in macrophage-derived foam cells, increased NEDD4 transcriptional activity, promoted ubiquitination of GATA4-p62 complex, and inhibited SASP-related inflammation. These findings suggest the potential of BBR as a novel approach to addressing SASP-associated inflammation in atherosclerosis.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"251-283"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143019247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Traditional Chinese Medicine for Alzheimer's Disease: A Systematic Review and Meta-Analysis.","authors":"Yuqing Chen, Danning Zhang, Teng Chen, Lixia Zhao, Lei Wen, Ruihua Hou","doi":"10.1142/S0192415X25500016","DOIUrl":"10.1142/S0192415X25500016","url":null,"abstract":"<p><p>The treatment of Alzheimer's Disease (AD) remains a challenge for modern medicine due to its complex pathogenesis. Traditional Chinese Medicine (TCM) has demonstrated significant success in the prevention and treatment of variable medical conditions. For AD pharmacological management, TCM could provide promising approaches. This study aimed to systematically evaluate the current evidence of the effects of TCM therapies on AD. A systematic search of the literature was performed on electronic databases including PubMed, the Cochrane Library, the Chinese National Knowledge Infrastructure (CNKI), and Web of Science. Thirteen studies were included in this review, subject to inclusion and exclusion criteria. Screening, data extraction, and quality assessment were undertaken following the guidelines for Preferred Reporting Items for Systematic Reviews and Meta-Analyses. Our results show that TCM offered a significant improvement in cognitive functioning compared to the control group, measured on both MMSE and ADAS-CoG scales, suggesting its potential utility in slowing cognitive decline and improving cognitive function as compared to conventional drug treatments and placebos. No significant difference was found for scores of neuropsychiatric symptoms (NPI) or ability to perform daily living activities (ADCS-ADL). These findings highlight TCM as a potential adjuvant therapy, in combination with conventional medicine, to improve the effectiveness and reduce the limitations of conventional AD drug regimes. Studies with larger sample sizes, rigorous study designs, accurate long-term reporting, and correlation to neuropathological markers are needed in the future to enhance the evidence base for the use of TCM in AD patients, and to further confirm its efficacy.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"53 1","pages":"1-15"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143506664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}