Chinese Medicine最新文献

{"title":"Triptolide targets PPP2CA/ITGA5 axis to suppress lactate-driven ovarian cancer progression.","authors":"Ling Ding, Wutao Chen, Cenxin Luo, Nathaniel Weygant, Yi Lai, Dan Ru, Hengan Liu, You Wang, He Li","doi":"10.1186/s13020-025-01174-2","DOIUrl":"10.1186/s13020-025-01174-2","url":null,"abstract":"<p><strong>Background: </strong>Triptolide, the active compound of Tripterygium wilfordii, exhibits broad anti-tumor activity. This study explores PPP2CA dysregulation in ovarian cancer (OC) progression via lactate production and evaluates Triptolide's potential to regulate this process.</p><p><strong>Methods: </strong>We used patient-derived xenograft (PDX) models, cell proliferation, and migration assays to assess lactate's impact on OC progression. CRISPR-Cas9 was applied to knock out PPP2CA, examining its effect on lactate production and tumor progression. RNA-seq analyzed transcriptomic changes post-PPP2CA knockout. The PPP2CA-ITGA5 axis was validated using xenografts, immunofluorescence, immunohistochemistry staining and western blot. Exosome isolation and co-culture experiments with tumor cells and human peritoneal mesothelial cells (HPMCs) investigated ITGA5's role in migration. Finally, patient-derived organoids, xenograft tumor model, and lactate assays assessed Triptolide's reversal effect on PPP2CA dysregulation-driven OC progression.</p><p><strong>Results: </strong>We found that PPP2CA dysregulation significantly promotes OC proliferation, migration, and tumorigenesis by enhancing YAP nuclear translocation and upregulating ITGA5/ITGB1. PPP2CA dysregulation led to ITGA5 upregulation, where ITGA5, as part of the integrin α5β1 heterodimer, plays a key role in driving OC migration. Exosomal ITGA5 facilitates OC metastasis to the HPMCs. Triptolide effectively inhibited patient-derived organoid growth and reduced lactate production in OC cells. By suppressing ITGA5, Triptolide reversed cancer progression and restored tumor-suppressive effects in a PPP2CA-knockout xenograft model.</p><p><strong>Conclusion: </strong>Our study reveals that Triptolide effectively inhibits OC progression by targeting the PPP2CA-ITGA5 axis, mitigating lactate-driven metabolic reprogramming.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"122"},"PeriodicalIF":5.7,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory mechanisms of hepatocyte PCSK9 expression: translating mechanistic insights into potential nutraceuticals.","authors":"Seon Kyeong Park, Jin-Taek Hwang, Hyo-Kyoung Choi, Jangho Lee","doi":"10.1186/s13020-025-01178-y","DOIUrl":"10.1186/s13020-025-01178-y","url":null,"abstract":"<p><p>Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a critical regulator of cholesterol metabolism in hepatocytes with profound implications for cardiovascular health. This review explores the intricate regulatory network that controls hepatic PCSK9 expression and explores how these molecular insights can be translated into nutraceutical applications. The precise control of PCSK9 involves complex interactions among transcription factors, signaling pathways, epigenetic modifications, and post-transcriptional mechanisms. Although pharmaceutical PCSK9 inhibitors demonstrated remarkable efficacy, their high cost has stimulated interest in natural alternatives. Bioactive compounds such as berberine, piceatannol, gallic acid, and organosulfur derivatives from garlic have demonstrated the ability to modulate PCSK9 expression through diverse mechanisms, often targeting the same molecular pathways as conventional drugs. These nutraceuticals not only inhibit PCSK9 but also enhance the expression and activity of the low-density lipoprotein receptor, offering a promising approach to reduce cardiovascular risk with potentially fewer side effects and greater accessibility. Understanding the precise mechanisms of these natural compounds advances the development of targeted dietary strategies to complement conventional pharmacotherapy in the treatment of hypercholesterolemia.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"121"},"PeriodicalIF":5.7,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Explore the potential mechanism of Huachansu injection against osteosarcoma via metabolomics, network pharmacology and bioinformatics.","authors":"Jingjing Meng, Xiangqi Zhang, Danfeng Xiang, Hanlu Liang, Shuai Zhao, Lingyan Xu, Jiao Yang, JunJun Chen, Jingxian Zhang, Yonglong Han","doi":"10.1186/s13020-025-01179-x","DOIUrl":"10.1186/s13020-025-01179-x","url":null,"abstract":"<p><strong>Aim: </strong>Huachansu injection (HCSI) shows effective medicinal functions against osteosarcoma. This study aimed to reveal the underlying mechanisms of HCSI against osteosarcoma by integrating metabolomics, network pharmacology and bioinformatics.</p><p><strong>Methods: </strong>Metabolomics was used to identify different metabolites and pathways. Network pharmacology was utilized to predict the potential targets of HCSI against osteosarcoma. Differentially expressed lncRNAs and miRNAs were screened and the corresponding lncRNAs-miRNAs-mRNAs network were constructed through the GEO database and miRcode database. Machine learning and immune infiltration analysis were performed on the key target obtained from the intersection of network pharmacology and bioinformatics. The binding affinity between active compounds of HCSI and potential targets was evaluated by molecular docking. The underlying mechanisms were further validated by RT-qPCR and immunoblotting.</p><p><strong>Results: </strong>Lipid metabolism pathways were obtained by non-target metabolomics enrichment. A total of 44 HCSI targets associated with osteosarcoma were collected by network pharmacology. Intersection of the mRNAs obtained from ceRNA network with the above 44 targets yielded eight common targets. The main target HMGCR were obtained by machine learning and RT-qPCR. The BCYRN1-miR-27a-3p-HMGCR axis was subsequently screened as the primary ceRNA regulatory network in HSCI against osteosarcoma. Molecular docking also showed an excellent affinity between the active compounds of HCSI and HMGCR. In vitro experiments demonstrated that HCSI down-regulated HMGCR, thereby reduced intracellular cholesterol levels, and ultimately promoting osteosarcoma cell apoptosis.</p><p><strong>Conclusion: </strong>HCSI could inhibit osteosarcoma progression by regulating lipid metabolism through BCYRN1-miR-27a-3p-HMGCR axis, indicating that HCSI may provide insights for developing herbal medicine injection-based therapies for osteosarcoma.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"120"},"PeriodicalIF":5.7,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Baitouweng decoction modulates gut microbial production of indole-3-propionic acid and epithelial necroptosis to alleviate DSS-induced colitis in mice.","authors":"Jingyi Hu, Hongxin Chen, Lei Zhu, Yiheng Tong, Cheng Cheng, Guoying Yan, Hong Shen","doi":"10.1186/s13020-025-01143-9","DOIUrl":"10.1186/s13020-025-01143-9","url":null,"abstract":"<p><strong>Background: </strong>Ulcerative colitis (UC) is a kind of inflammatory disorder structuring in the colon. Baitouweng decoction (BD) derived from Treatise on Cold Damage (Shang-Han-Lun in Chinese) has been used for the treatment of UC in clinical practice for more than 2000 years. However, the clear mechanism of BD is still unknown. Our previous study revealed the regulation of BD on gut microbiota in colitis mice. This study aimed to investigate the crosstalk between intestinal flora and host immunity in the therapeutic effect of BD on colitis.</p><p><strong>Methods: </strong>The model of colitis in mice was established using dextran sulfate sodium in drinking water, and the treatment group received BD, 5-ASA, or indole-3-propionic acid (IPA). The disease symptoms were documented, and assessments were conducted on both local and systemic inflammation as well as intestinal barrier function. The gut microbiota structure was analyzed using 16S ribosomal RNA sequencing. The metabolomic assay was performed using ultra-high performance liquid chromatography and quadrupole time-of-flight mass spectrometry, and RNA-sequencing was used to explore the mechanism of IPA on colitis treatment.</p><p><strong>Results: </strong>BD could improve colitis mice's colonic injury and rebalance the gut microbiota dysbiosis. Fecal microbiota transplantation experiments confirmed that the therapeutic effects of BD depend on the intestinal flora, while antibiotic treatment abrogated the effect of BD. The concentration of IPA, a microbial tryptophan metabolite, was upregulated after BD-treated. IPA was further evaluated for its effect on the development of colitis and it was identified as an inhibitor of necroptosis of intestinal epithelial cells.</p><p><strong>Conclusions: </strong>Our findings suggest that BD could alleviate colitis by regulating the gut microbiota-metabolism homeostasis to inhibit the necroptosis of intestinal epithelial cells.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"119"},"PeriodicalIF":5.7,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12312286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Filiform fire needling therapy relieves T cells-mediated melanocyte apoptosis and dysfunction by inhibiting JAK/STAT3 pathway via Mfsd4a in vitiligo.","authors":"Yue Shi, Dong Chen, Yao Wang, Cong Zhang, Yana Cao, Yan Liu, Ting Song, Cheng Tan, Yongjun Peng","doi":"10.1186/s13020-025-01172-4","DOIUrl":"10.1186/s13020-025-01172-4","url":null,"abstract":"<p><p>We investigated the molecular mechanism of filiform fire needling therapy (FFN), an effective treatment option for vitiligo, focusing on its role in relieving depigmentation. Firstly, we validated the efficacy and safety of FFN in a study with 11 enrolled vitiligo patients. We then found that the depigmentation score was significantly improved in monobenzone-induced vitiligo mice treated with FFN. Subsequently, after being co-cultured with T-cells extracted from FFN-treated lesions, apoptosis of melanocytes was reduced and melanogenesis was enhanced. Furthermore, the gene Mfsd4a was significantly differentially expressed in melanocytes between the model group and the FFN intervention group. Further in vitro verification showed that JAK/STAT3 pathway activity was inhibited, and melanocyte activity was enhanced after knocking out Mfsd4a in co-cultured melanocytes from the monobenzone group. Moreover, interference with Mfsd4a increased MITF transcription, leading to TYR activation and promotion of melanin formation. Lastly, we found that IL-6 was involved in regulating Mfsd4a-mediated JAK/STAT3 pathway suppression, thereby regulating melanocyte survival and melanogenesis. These results demonstrate that FFN alleviates T cell-mediated melanocyte apoptosis and dysfunction by inhibiting the JAK/STAT3 pathway signaling pathway via Mfsd4a to treat vitiligo.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"117"},"PeriodicalIF":5.7,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12288293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Qu-zhuo-tong-bi decoction exerts gouty arthritis therapy by skewing macrophage polarization through butanoate metabolism.","authors":"Siyue Song, Xianghui Wen, Fusen Chen, Jiatao Li, Kaiyue Shi, Yu Lou, Anyi Xu, Chengping Wen, Tiejuan Shao","doi":"10.1186/s13020-025-01162-6","DOIUrl":"10.1186/s13020-025-01162-6","url":null,"abstract":"<p><strong>Background: </strong>Qu-zhuo-tong-bi decoction (QZTBD), a traditional Chinese medicine (TCM), has demonstrated efficacy in the treatment of gouty arthritis. However, to date, the precise pharmacological mechanisms remain unclear.</p><p><strong>Purpose: </strong>The study aims to ascertain the therapeutic effects and the underlying mechanisms of QZTBD in the treatment of gouty arthritis.</p><p><strong>Methods: </strong>The efficacy and safety of different doses of QZTBD were investigated in Uox-KO mice. Candidate active ingredients were identified using UHPLC-MS/MS. The potential therapeutic pathways of the active ingredients were predicted through network pharmacology. The mechanisms of QZTBD in alleviating gouty arthritis were explored via comprehensive analyses of gut microbiota, combined with RT-qPCR, western blot, immunofluorescence, ELISA, flow cytometry, and Seahorse assay. Fecal microbiota transplantation (FMT), bacterial culture experiment, butyrate-producing bacteria (BPB) and butyrate administration, and 2-DG intervention were conducted to explore the roles of BPB and butanoate metabolism in gout progression and therapeutic mechanisms of QZTBD. In vitro studies further validated the regulatory effects of butyrate and QZTBD on macrophage polarization through glycolysis modulation.</p><p><strong>Results: </strong>18.0 g/kg/d of QZTBD effectively alleviated the symptoms of gouty arthritis with excellent hepatic and renal safety. UHPLC-MS/MS analysis and network pharmacology revealed that QZTBD exerts its effects on butanoate metabolism during gouty arthritis inflammation. QZTBD treatment increased the abundance of BPB, the levels of serum and colon butyrate, and the expression levels of Buk and But. The transplantation of QZTBD-treated microbiota reproduced the therapeutic effects of QZTBD. M1 macrophage polarization was suppressed after QZTBD intervention. The administration of BPB and butyrate attenuated gouty arthritis and orchestrated macrophage polarization. Inhibition of glycolysis regulated the phenotype of macrophage and attenuated inflammatory processes. In vitro analysis unveiled that QZTBD and butyrate modulated glycolysis to regulate macrophage polarization, thereby alleviating gouty arthritis.</p><p><strong>Conclusion: </strong>QZTBD targeted butanoate metabolism to regulate macrophage polarization, thereby effectively alleviating intestinal inflammation and restoring immune homeostasis in gouty arthritis. These findings establish a mechanistic foundation for developing precision therapeutic strategies leveraging QZTBD to combat gouty arthritis.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"115"},"PeriodicalIF":5.7,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12281712/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144689077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A review of acupoint localization based on deep learning.","authors":"Jiahao Li, Zhennan Fei, Yingjiang Xie, Da Deng, Xingcheng Ming, Fu Niu","doi":"10.1186/s13020-025-01173-3","DOIUrl":"10.1186/s13020-025-01173-3","url":null,"abstract":"<p><p>The development of deep learning has brought unprecedented opportunities for automatic acupoint localization, surmounting many limitations of traditional methods and machine learning, and significantly propelling the modernization of Traditional Chinese Medicine (TCM). We comprehensively review and analyze relevant research in this field in recent years, and examine the principles, classifications, commonly used datasets, evaluation metrics and application fields of acupoint localization algorithms based on deep learning. We categorize them by body part, algorithm architecture, localization strategy, and image modality, and summarize their characteristics, pros and cons, and suitable application scenarios. Then we sieve out representative datasets of high value and wide application, and detail some key evaluation metrics for better assessment. Finally, we sum up the application status of current automatic acupoint localization technology in various fields, hoping to offer practical reference and guidance for future research and practice.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"116"},"PeriodicalIF":5.7,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12281682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144689076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating multi-omics and machine learning strategies to explore the \"gene-protein-metabolite\" network in ischemic heart failure with Qi deficiency and blood stasis syndrome.","authors":"Jingjing Wei, Aolong Wang, Peng Yu, Yang Sun, Wenjun Wu, Yilin Zhang, Rui Yu, Bin Li, Mingjun Zhu","doi":"10.1186/s13020-025-01151-9","DOIUrl":"10.1186/s13020-025-01151-9","url":null,"abstract":"<p><strong>Background: </strong>Ischemic heart failure (IHF) is a multifaceted syndrome associated with significant mortality and high hospitalization rates globally. According to traditional Chinese medicine (TCM) theory, Qi Deficiency and Blood Stasis (QXXY) Syndrome serves as the pathological basis of IHF. This study aims to investigate the biological basis of QXXY syndrome in IHF patients through an integrated multi-omics approach.</p><p><strong>Methods: </strong>We enrolled 100 participants, comprising 40 IHF patients with QXXY syndrome (IHF-QXXY), 40 IHF patients without QXXY syndrome, and 20 healthy controls. Utilizing an integrated approach combining RNA sequencing (RNA-seq), data-independent acquisition (DIA) proteomics, and targeted metabolomics, we established a comprehensive \"gene-protein-metabolite\" network for IHF-QXXY syndrome. Candidate biomarkers were identified through machine learning algorithms and further validated using RT-qPCR and targeted proteomics via intelligent parallel reaction monitoring (iPRM).</p><p><strong>Results: </strong>Patients with IHF-QXXY syndrome present with pronounced disruptions in energy metabolism, chronic inflammation, and coagulation abnormalities. The \"gene-protein-metabolite\" network of IHF-QXXY syndrome comprises six mRNAs, four proteins, and five metabolites. Key pathways involve the activation of neutrophil extracellular traps formation, platelet activation, the HIF-1 signaling pathway, and glycolysis/gluconeogenesis, alongside the suppression of the citrate cycle and oxidative phosphorylation. The key metabolites potentially associated with QXXY syndrome include 3-methylpentanoic acid, arachidonic acid, N-acetylaspartylglutamic acid, L-acetylcarnitine, and 12-hydroxystearic acid. We identified a panel of candidate biomarkers, including HIF-1α, IL10, PAD4, ACTG1, SOD2, GAPDH, FGA, FN1, F13A1, and ATP5PF. This biomarker combination significantly enhanced the diagnostic performance of IHF-QXXY syndrome (AUC > 0.863) and retained high diagnostic accuracy during validation (AUC > 0.75).</p><p><strong>Conclusion: </strong>This study provides a comprehensive characterization of the molecular features of QXXY syndrome in IHF patients, highlighting key pathways and biomarkers linked to energy metabolism dysregulation, chronic inflammation, and coagulation abnormalities. These findings may provide novel insights and methods for further advancing this research field.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"93"},"PeriodicalIF":5.3,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269143/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The emerging role of mitochondria in the pharmacological and toxicological effects of Tripterygium wilfordii Hook F: functions, targets and new therapeutic applications.","authors":"Zhonghao Liu, Dan Li, Xiongwen Yang, Xisha Chen, Chengxiao Fu","doi":"10.1186/s13020-025-01170-6","DOIUrl":"10.1186/s13020-025-01170-6","url":null,"abstract":"<p><p>Tripterygium wilfordii Hook F (TWHF) is a traditional Chinese medicine with multifaceted pharmacological properties, has faced clinical application challenges due to its dose-limiting organ toxicity. Through a systematic analysis of current literature, this review deciphers the dual regulatory role of mitochondrial function in mediating both therapeutic efficacy and adverse effects of TWHF-derived active compounds. We elucidate that processes such as mitochondrial biogenesis, mitochondrial fusion and fission, mitophagy and mitochondrial apoptosis pathways influence the therapeutic efficacy and adverse effects of TWHF active ingredients. In addition, we review innovative dosage forms and derivatives of TWHF that exploit mitochondrial targeting to enhance their pharmacological efficacy. This article offers a concise overview pharmacological and toxicological effects of the principal active components of TWHF, in particular triptolide and celastrol, with a particular emphasis on elucidating the critical role of mitochondria in these processes. Further high-quality basic studies are essential to strengthen the link between mitochondrial function and the active compounds of TWHF, offering more diverse options for their clinical development.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"114"},"PeriodicalIF":5.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12265187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aster tataricus extract and its active compounds display a broad spectrum of antiviral activity in vitro and in vivo.","authors":"Nuwan Gamage, Ji-Won Cha, Ji-Soo Jeong, Yebin Seong, Kiramage Chathuranga, Asela Weerawardhana, Jin Yeul Ma, Tae-Won Kim, Jong-Soo Lee","doi":"10.1186/s13020-025-01167-1","DOIUrl":"10.1186/s13020-025-01167-1","url":null,"abstract":"<p><strong>Background: </strong>Aster tataricus, a perennial terrestrial herb with a rich history of use in traditional medicine, is renowned for its therapeutic properties. However, despite the widespread use of Aster tataricus, its antiviral efficacy and mode of action against viruses have not yet been studied. Here, we demonstrated that Aster tataricus extract (ATE) has antiviral effects and an underlying mechanism of action both in vitro and in vivo.</p><p><strong>Methods: </strong>Antiviral effect of ATE was assessed against Influenza A virus (PR8), Newcastle Disease Virus (NDV), and Herpes Simplex Virus-1 (HSV) in RAW264.7 cells. Mechanism was explored by analyzing the induction of antiviral immune responses, including type-I interferon (IFN) signaling and cytokine secretion. In vivo, BALB/c mice were treated with ATE prior to infection with lethal influenza A subtypes, A/PR/8/34 (H1N1), A/Aquatic bird/Korea/W81/2005 (H5N2), and A/Chicken/Korea/116/2004 (H9N2). Survival rates, viral titers, and lung pathology were measured. High-performance liquid chromatography (HPLC) was used to identify active compounds in ATE, and their antiviral effects were further investigated.</p><p><strong>Results: </strong>An effective dose of ATE significantly inhibited influenza A virus (PR8), NDV, and HSV replication in RAW264.7 cells. Mechanistically, we found that ATE induced an antiviral state, which includes upregulation of type-I interferon signaling and secretion of IFNs and pro-inflammatory cytokines in RAW264.7 cells. In vivo, ATE treatment showed increased survival due to reduced viral titers and less severe pathological changes in the lung, and the observed prophylactic effects were associated with increased secretion of IL-6, IFN-γ, and IFN-β in bronchoalveolar lavage fluid. Based on the reported information and HPLC analysis, quercetin, kaempferol, and ferulic acid were identified as active compounds in the aqueous fraction, and an effective dose of each compound exhibited antiviral effects similar to ATE against influenza viruses.</p><p><strong>Conclusions: </strong>These findings suggest that ATE and its active compounds act as immunomodulators and may be potential candidates as a source of promising natural antivirals for animals and humans.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"113"},"PeriodicalIF":5.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12265312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}