Chinese Medicine最新文献

{"title":"Natural product library screening identifies Darutigenol for the treatment of myocardial infarction and ischemia/reperfusion injury.","authors":"Kun Liu, Li Zheng, Qian-Yu Huang, Hong-Ji Li, Cheng Li, Hui Zhao, Ze-Bing Ye, Hao Wang, Xu-Feng Qi, Meng Wang","doi":"10.1186/s13020-025-01141-x","DOIUrl":"10.1186/s13020-025-01141-x","url":null,"abstract":"<p><strong>Introduction: </strong>Ischemic heart diseases are the leading cause of death worldwide due to the inability of regeneration of adult cardiomyocytes (CMs). Natural products from medical herbs are an important source of innovative drugs for many diseases including cardiovascular diseases.</p><p><strong>Objectives: </strong>In this study, we set out to screen novel small-molecule therapies from natural products to protect heart against ischemic injury.</p><p><strong>Methods: </strong>High-throughput screening was performed using a natural product library to identify the potential small molecules which can promote survival of CMs under ischemic and ischemic/reperfusion conditions. In addition, myocardial infarction (MI) and ischemia/reperfusion (I/R) mice models were used to evaluate the in vivo effects of the screened candidate. We also applied various analysis including cell viability, qPCR, Western blot, immunofluorescent staining, echocardiography, Masson's staining, TTC staining, and network pharmacology.</p><p><strong>Results: </strong>High-throughput screening showed that the small molecule compound Darutigenol (Dar), derived from the Chinese traditional herb Herba Siegesbeckiae, could significantly promote CM survival and proliferation under ischemic conditions. Moreover, I/R-induced CM apoptosis and ROS generation could be significantly reduced by Dar treatment. In addition, in vivo administration of Dar was able to attenuate MI- and I/R-induced cardiac injury in adult mice by decreasing fibrosis and apoptosis, thereby improving cardiac function. Network pharmacology analysis and molecule docking assay showed that Dar has the highest binding affinity with AKT1 protein. Western blotting assay further revealed that AKT1 activation was significantly enhanced by Dar administration in the infarcted hearts.</p><p><strong>Conclusions: </strong>Our data revealed that the small molecule compound Dar, screened from the natural product library in this study, is capable of protecting heart against MI and I/R injury by activating AKT1 pathway. These findings enrich the natural product candidates for cardiovascular disease treatment and provide new insights into potential therapeutic agents for MI and I/R injury.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"90"},"PeriodicalIF":5.3,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12175470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324610","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":"Wenshen Zhuanggu formula inhibits tumor-exosomes induced bone pre-metastasis niche formation in primary breast cancer mice.","authors":"Qionglian Huang, Hanjuan Ning, Jue Wang, Weiwei Liu, Sheng Liu, Jianyi Wang, Xianghui Han","doi":"10.1186/s13020-025-01136-8","DOIUrl":"10.1186/s13020-025-01136-8","url":null,"abstract":"<p><strong>Background: </strong>The therapy for breast cancer bone metastasis (BCBM) still needs profound investigation. Focusing on the formation of bone pre-metastasis niche (BPMN) is a crucial tache for BCBM treatment. Wenshen Zhuanggu Formula (WSZG) is a typical traditional Chinese medicine (TCM) prescription with ability of clinically palliating bone pain and ameliorating the quality of life of BCBM patients. This study aims to elucidate the inhibitory effect and underlying mechanism of WSZG on BPMN formation induced by tumor-derived exosomes.</p><p><strong>Methods: </strong>Bone precursor cells were exposed to exosomes derived from MDA-MB-231BO cells (BO-exo, 50 μg/mL) and treated by WSZG (10 or 20 μg/mL) in vitro. A primary breast cancer mouse model with propensity of BPMN was established by pre-educating BO-exo and then subcutaneously injecting MDA-MB-231BO cells into mammary fat pads. After the modeled mice were orally administrated WSZG (6.5 or 13 g crude herb kg^-1 d^-1) for 28 days, bone architecture and bone parameters of tibia were analyzed using micro-CT. The absorbed exosomes by bone precursor cells were investigated using confocal microscopy. Osteoclastic and osteoblastic differentiation were examined by TRAP, ALP and qRT-PCR. The levels of protein related to bone metabolism and extracellular matrix (ECM) were detected by ELISA and IHC methods.</p><p><strong>Results: </strong>The results showed that BO-exo elicited the vicious bone microenvironment to form BPMN in bone-tropic primary BC mice. WSZG encouragingly targeted BO-exo to hinder osteoclastic differentiation (ACP5, c-Fos, Ctsk, MMP9, NFATc1), improve focal bone lesions (BMD, Tb.N, Tb.Th, Tb.Sp, Conn-Dens. and BV/TV), and downregulate the expression levels of bone metabolism markers (ICTP, BALP, TRACP-5b) and bone ECM proteins (bone sialoprotein, elastin, fibronectin, osteopontin, collagen I and vitronectin).</p><p><strong>Conclusions: </strong>This study denotes the enhanced effects of BO-exo and highly inhibitive possibility by WSZG treatment on BPMN formation, shaping bone metastatic landscape of BC and informing the treatment of early-stage BCBM in terms of TCM.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"88"},"PeriodicalIF":5.3,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12168286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309590","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":"Quercetagetin alleviates liver fibrosis in non-alcoholic fatty liver disease by promoting ferroptosis of hepatic stellate cells through GPX4 ubiquitination.","authors":"Yuping Qiu, Shupei Li, Mingzuo Jiang, Ang Huang, Ya Yang, Xi Chen, Hui Li, Zhizhou Yang, Juan Wei, Ji Xuan","doi":"10.1186/s13020-025-01109-x","DOIUrl":"10.1186/s13020-025-01109-x","url":null,"abstract":"<p><strong>Background: </strong>Lang Qing A Ta (Huagan Tongluo Fang, HGTLF) is a Tibetan medicine with significant anti-liver fibrosis effects and good efficacy in the treatment of liver diseases, including non-alcoholic fatty liver disease (NAFLD). Quercetagetin (QG) has been identified as an active ingredient of HGTLF that is absorbed into the blood. This study aims to investigate the role of QG in the anti-liver fibrosis effect of HGTLF in NAFLD.</p><p><strong>Methods: </strong>CCl₄ injection-induced liver fibrosis and high-fat, high-cholesterol diet-induced non-alcoholic steatohepatitis (NASH) mouse models were established. Transforming growth factor-β1 (TGF-β1)-induced hepatic stellate cells (HSCs) were used as in vitro models. The effect of QG on the stability and degradation pathway of glu-tathione peroxidase 4 (GPX4) protein was investigated.</p><p><strong>Results: </strong>QG improved liver function and hyperlipidemia in CCl₄-injected mice and NASH mice, and alleviated hepatic lipid deposition and hepatic fibrosis. TGF-β1 treatment promoted the expression of α-smooth muscle actin and fibrosis-related genes, while QG reversed this phenomenon and inhibited HSC activation. QG increased the intracellular labile iron pool and lipid reactive oxygen species in HSCs. Treatment with the ferroptosis inhibitor ferrostatin-1 reversed the inhibitory effect of QG on TGF-β1-induced HSC activation. QG reduced GPX4 protein stability and regulated GPX4 K167 ubiquitination via the membrane-associated ring-CH-type finger 8 (MARCHF8)-mediated ubiquitin-proteasome pathway. Interference with MARCHF8 attenuated the effect of QG and promoted HSC activation induced by TGF-β1.</p><p><strong>Conclusion: </strong>QG, the active ingredient of HGTLF, can induce ferroptosis of HSCs by targeting the degradation of GPX4 through ubiquitination and inhibit HSC activation, thereby alleviating liver fibrosis in NAFLD.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"89"},"PeriodicalIF":5.3,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12168282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309570","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":"Dingzhen pills inhibit neuronal ferroptosis and neuroinflammation by inhibiting the cGAS-STING pathway for Parkinson's disease mice.","authors":"Gaoshuang Fu, Ting Li, Yukun Zhao, Shuai Zhang, Xin Xue, Yuqin Yang, Tingyu Li, Shaohan Luo, Guangxin Yue, Tong Lei","doi":"10.1186/s13020-025-01135-9","DOIUrl":"10.1186/s13020-025-01135-9","url":null,"abstract":"<p><strong>Background: </strong>Parkinson's disease (PD) is a neurodegenerative disease whose cause and molecular mechanism remain unclear. Dingzhen pill (DZP), a water extract from crude herbs, is thought to possibly play a neuroprotective role in PD. However, the underlying pharmacological mechanisms of the DZP and its impact on the potential pathways against PD have not been elucidated.</p><p><strong>Aim: </strong>The aim of this study was to explore the effect and molecular mechanism of DZP treatment on PD by quantitative proteomic and metabolomic analysis.</p><p><strong>Methods: </strong>The effect of DZP on the behavior of movement disorders in a mouse model of MPTP-induced was first evaluated. Secondary metabolomics for TCM resolved the components of DZP and its metabolites distributed in the serum of PD mice. Proteomics was used to resolve the effects of DZP on proteins in brain tissue in mice with PD. Network pharmacology and molecular docking analysis were used to screen and validate the binding relationships of components and targets. Immunofluorescence and western blot analysis verified the pathway affected by DZP.</p><p><strong>Results: </strong>Our study showed that DZP improved the movement disorder of PD mice and promoted the recovery of dopaminergic neurons in substantia nigra. Secondary metabolomics showed that 460 kinds of secondary metabolites existed in serum of PD mice after DZP treatment. Proteomics analysis showed that DZP affected the expression of 9393 proteins, 87 of which were up-regulated and 120 down-regulated. Through target prediction and molecular docking, a total of 8 compounds were found to interact with 8 pathological PD targets, playing a significant role in neuronal protection. In addition, DZP inhibits neuronal ferroptosis and neuroinflammation by inhibiting the cGAS-STING pathway.</p><p><strong>Conclusion: </strong>This study is helpful to understand the molecular mechanism of the multi-component, multi-target neuroprotective effect of DZ, and may contribute to the development of DZP as a new therapeutic strategy for clinical application in PD.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"87"},"PeriodicalIF":5.3,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12168260/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309569","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":"Senkyunolide I suppresses hepatic stellate cell activation and liver fibrosis by reprogramming VDR-dependent fatty acid metabolism.","authors":"Mengyao Zhu, Lu Ren, Wenlong Xiao, Longjian Wang, Zhiming Hu, Nani Wang","doi":"10.1186/s13020-025-01133-x","DOIUrl":"10.1186/s13020-025-01133-x","url":null,"abstract":"<p><p>Hepatic stellate cells (HSCs) activation represents a central pathological mechanism in liver fibrosis, with emerging evidence implicating fatty acid metabolic reprogramming as a critical regulator of this process. Our study established the vitamin D receptor (VDR) as a key transcriptional coordinator of fatty acid metabolism during HSC activation. Genetic VDR deletion in mice exacerbated liver fibrosis progression, which was associated with elevated TGF-β1 levels and increased Smad3 phosphorylation. Mechanistically, VDR deficiency disrupted lipid homeostasis through the upregulation of lipogenic enzymes (fatty acid synthase, acetyl-CoA carboxylase 1, ATP citrate lyase) and desaturases (stearoyl-CoA desaturase-1, fatty acid desaturases 1/2) and the suppression of the β-oxidation gatekeeper carnitine palmitoyltransferase 1A (CPT1A). Pathological VDR downregulation was observed in both TGF-β1-activated HSCs and fibrotic liver tissues, suggesting a disease-associated regulatory circuit. Calcitriol-mediated VDR activation reversed TGF-β1-induced Smad3 phosphorylation and normalized metabolic enzyme expression, effectively reducing lipid accumulation and collagen deposition. We further identified senkyunolide I as a novel natural VDR agonist that rebalances fatty acid metabolism by simultaneously downregulating lipogenesis/desaturation machinery and upregulating CPT1A. The complete abolition of anti-fibrotic effects of senkyunolide I following VDR knockdown confirmed its strict receptor dependency. These findings identify VDR as a master regulator of metabolic reprogramming in HSC activation and validate pharmacological VDR activation as a promising therapeutic strategy for liver fibrosis. The dual metabolic regulatory capacity of senkyunolide I through VDR signaling highlights its potential for targeted antifibrotic intervention.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"85"},"PeriodicalIF":5.3,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12164082/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293446","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":"Ginsenoside Rg5 alleviates hypoxia-induced myocardial apoptosis by targeting STAT3 to promote Tyr705 phosphorylation.","authors":"Fang-Yang Li, Yi-Hao Wang, Cheng Zhang, Wan-Yun Dang, Ze-Kun Wu, Zhen-Hui Wu, Jia-Lu Cui, Xiang-Jun Wu, Chun-Qi Yang, Xue-Cong Tian, Cheng-Rong Xiao, Yu-Guang Wang, Yue Gao","doi":"10.1186/s13020-025-01128-8","DOIUrl":"10.1186/s13020-025-01128-8","url":null,"abstract":"<p><strong>Background: </strong>The heart, as the body's blood-pumping organ, is extremely sensitive to changes in oxygen levels. Myocardial injury caused by hypoxia is a challenging issue, and there are currently no definitive specific drugs available for its treatment. Ginsenoside Rg5, one of the main rare saponins in ginseng, has shown significant efficacy in treating myocardial injury. This study aims to investigate the role and mechanisms of Rg5 in the treatment of hypoxic myocardial injury.</p><p><strong>Methods: </strong>The cardioprotective effect against acute hypoxia of Rg5 was studied by assessing heart function, myocardial injury markers, inflammation, and oxidative stress in C57 mice, as well as apoptosis and reactive oxygen species (ROS) levels in H9c2 cardiomyocytes. Thermal proteome and target validation techniques were used to confirm the target protein of Rg5. The further protective mechanisms against hypoxia-induced damage were explored using immunocoprecipitation, immunofluorescence and rescue experiments in vivo and in vitro.</p><p><strong>Results: </strong>The experimental results demonstrated that Rg5 effectively improved cardiac function in mice, reduced inflammation, oxidative stress, and the release of myocardial injury markers, decreased cardiomyocyte apoptosis, and lowered ROS levels. Further, using target protein screening and validation techniques, Signal transducer and activator of transcription 3 (STAT3) was verified as a direct target for Rg5's cardioprotective effect. It was observed that Rg5 specifically promoted the phosphorylation of Tyr705 in STAT3 via the JAK2/STAT3 pathway, leading to the translocation of phosphorylated STAT3 into the nucleus where they induce the expression of anti-apoptotic protein and protect cells from hypoxic damage.</p><p><strong>Conclusion: </strong>Rg5 could be a potential therapeutic agent for preventing and treating myocardial hypoxic injury, providing scientific evidence for its application in anti-hypoxic therapy.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"86"},"PeriodicalIF":5.3,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12166643/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293445","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":"Study on a Traditional Chinese Medicine constitution recognition model using tongue image characteristics and deep learning: a prospective dual-center investigation.","authors":"Yongyue Liu, Linmiao Fan, Mei Zhao, Dongshen Wei, Menglan Zhao, Yihang Dong, Xiaoqing Zhang","doi":"10.1186/s13020-025-01126-w","DOIUrl":"10.1186/s13020-025-01126-w","url":null,"abstract":"<p><strong>Purpose: </strong>The objective of this study was to develop a quantitatively analyzed Traditional Chinese Medicine (TCM) constitution recognition model utilizing tongue fusion features and deep learning techniques.</p><p><strong>Methods: </strong>A prospective investigation was conducted on participants undergoing TCM constitution assessment at two medical centers. Tongue images and corresponding TCM constitution data were collected from 1374 participants using specialized equipment. Both traditional and deep features were extracted from these images. Significant features associated with constitutional characteristics were identified through LASSO regression and Random Forest (RF). Eight machine learning algorithms were employed to construct and evaluate the efficacy of the models. The highest-performing model was selected as the foundational classifier for developing an integrated tongue image feature model. Model performance was comprehensively evaluated using accuracy, precision, recall, F1 score, and area under the curve (AUC).</p><p><strong>Results: </strong>Analysis revealed 11 critical traditional tongue image features and 26 deep tongue image features. Three datasets were constructed: traditional tongue image features, deep tongue image features, and a fusion feature dataset incorporating both. The multilayer perceptron (MLP) model combining traditional and deep features demonstrated superior performance in TCM constitution classification compared to single-feature models. In the training phase, the model achieved an accuracy (ACC) of 0.893 and an AUC of 0.948. On the test set, it achieved an ACC of 0.837 and an AUC of 0.898, with sensitivity and specificity of 0.680 and 0.930, respectively, indicating excellent generalization ability.</p><p><strong>Conclusions: </strong>This study successfully developed an intelligent TCM constitution recognition model that overcomes the limitations of traditional methods and validates the value of tongue images for accurate constitution recognition.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"84"},"PeriodicalIF":5.3,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12160370/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282714","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 gut microbiota-mediated ferroptosis pathway: a key mechanism of ginsenoside Rd against metabolism-associated fatty liver disease.","authors":"Wenjing Liu, Xian Zhou, Liyu Xiao, Xiaolan Huang, Dennis Chang, Xiaomei Zhong, Minjie Zeng, Yanfang Xian, Yanfang Zheng, Wei Huang, Rui Huang, Mingqing Huang","doi":"10.1186/s13020-025-01121-1","DOIUrl":"10.1186/s13020-025-01121-1","url":null,"abstract":"<p><strong>Background: </strong>Ginsenoside Rd (G-Rd), found in Panax species, has shown therapeutic potential against metabolism-associated fatty liver disease (MAFLD), but its mechanism has not been well elucidated. This study investigated the key mechanisms of G-Rd in modulating the gut microbiome and lipid peroxidation-mediated ferroptosis pathway in MAFLD.</p><p><strong>Methods: </strong>A high-fat diet-induced MAFLD model was established. Ultrastructural changes in liver tissue were observed using transmission electron microscopy. Metagenomics were employed to detect alterations in gut microbiota and their metabolites. Biochemical analysis and immunohistochemistry were used to examine liver injury, blood lipids, lipid peroxidation-related indicators, and tissue iron content.</p><p><strong>Results: </strong>G-Rd significantly reduced liver injury and steatosis in MAFLD mice and downregulated the elevated relative abundance of Firmicutes and the Firmicutes/Bacteroidetes ratio. It also significantly reduced the abundances of Faecalibaculum rodentium while increasing Muribaculum intestinale, with its functional role being relevant to lipid metabolism regulation. Moreover, G-Rd ameliorated mitochondrial damage and inhibited the ferroptosis pathway in the liver, which was associated with antioxidant-related factors mediated by Nrf2 signaling. The liver protective effect of G-Rd was driven by the regulation of gut microbiota, as demonstrated by antibiotic cocktail treatment and fecal microbiota transplantation.</p><p><strong>Conclusions: </strong>G-Rd attenuated HFD-induced MAFLD by alleviating liver oxidative stress, lipid peroxidation, and ferroptosis through modulation of the gut microbiota. The antioxidant and anti-ferroptotic actions of G-Rd, mediated via the Nrf2 pathway, were found to contribute to the amelioration of liver injury and hepatic steatosis in MAFLD.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"83"},"PeriodicalIF":5.3,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12150452/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265412","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":"Natural anti-cancer products: insights from herbal medicine.","authors":"Dianxin Cui, Cheng Zhang, Lili Zhang, Jingbin Zheng, Jie Wang, Luying He, Haochun Jin, Qianming Kang, Yang Zhang, Na Li, Zhenlong Sun, Wenying Zheng, Jinchao Wei, Siyuan Zhang, Yibin Feng, Wen Tan, Zhangfeng Zhong","doi":"10.1186/s13020-025-01124-y","DOIUrl":"10.1186/s13020-025-01124-y","url":null,"abstract":"<p><p>Herbal medicine exhibits a broad spectrum of potent anti-cancer properties, including the enhancement of tumor immune responses, reversal of multidrug resistance, regulation of autophagy and ferroptosis, as well as anti-proliferative, pro-apoptotic, and anti-metastatic effects. This review systematically explores recent advances (primarily documented since 2019) in research on key anti-cancer compounds derived from herbal medicine, such as apigenin, artemisinin, berberine, curcumin, emodin, epigallocatechin gallate (EGCG), ginsenosides, icariin, resveratrol, silibinin, triptolide, and ursolic acid (UA). These studies were sourced from scientific databases, including PubMed, Web of Science, Medline, Scopus, and Clinical Trials. The review focuses on the significant role that these natural products play in modern oncology, exploring their efficacy, mechanisms of action, and the challenges and prospects of integrating them into conventional cancer therapies. Furthermore, it highlights cutting-edge approaches in cancer research, such as the utilization of gut microbiota, omics technologies, synthetic derivatives, and advanced drug delivery systems (DDS). This review underscores the potential of these natural products to advance the development of novel anti-cancer treatments and support contemporary medicine. Additionally, recent multi-omics findings reveal how these compounds reshape transcriptional and metabolic networks, further broadening their therapeutic scope. Many natural products exhibit synergy with first-line chemotherapies or targeted therapies, thereby enhancing treatment efficacy and reducing side effects. Advanced nano-formulations and antibody-drug conjugates have also substantially improved their bioavailability, making them promising candidates for future translational research.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"82"},"PeriodicalIF":5.3,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12147394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257451","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":"Unveiling the immunopharmacological mechanisms of Danggui Yinzi (DGYZ) in treating chronic urticaria: insights from network pharmacology and experimental validation.","authors":"Xu-Rui Wang, An-Jing Chen, Chang-Cheng Hou, Yue-Yue Wang, Jing Guo, Ming-Yue Li","doi":"10.1186/s13020-025-01137-7","DOIUrl":"10.1186/s13020-025-01137-7","url":null,"abstract":"<p><strong>Background: </strong>Chronic urticaria (CU), a prevalent and often debilitating allergic skin disorder, is primarily triggered by mast cell degranulation. Danggui Yinzi (DGYZ), a traditional Chinese medicine formula, has been employed to treat pruritic conditions. However, the molecular mechanisms underlying its effects in CU remain unclear. This study aimed to investigate the immunopharmacological mechanisms of DGYZ in CU, hypothesizing that it modulates immune responses through its bioactive components, which is critical for the development of novel therapeutic agents.</p><p><strong>Methods: </strong>Ultra-performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry (UPLC-Q-TOF-MS) was used to identify the active compounds in DGYZ. In vivo, BALB/c mouse models of DNP-IgE/DNFB-induced CU were established and grouped into Normal Control (NC), Model, various-dose DGYZ, and Loratadine groups. Post-treatment, immunopharmacological parameters were assessed, and skin tissue was collected for histopathological analysis, mast cell quantification, and immunohistochemistry to evaluate the impact on immune cells and molecules. Serum levels of inflammatory cytokines (TNF-α, IL-6) were quantified using ELISA kits. In vitro, the human mast cell line LAD2 was pretreated with key active components of DGYZ (Quercetin and Paeoniflorin) at different concentrations before mast cell degranulation was induced. Degranulation markers (β-HEX, HIS) and the expression of proteins in immune-related signaling pathways (PI3K-Akt, TLR4) were then measured.</p><p><strong>Results: </strong>A total of 38 active components were identified in DGYZ. In vivo, DGYZ inhibited mast cell degranulation, blue spot reactions, and skin damage in mice. It also decreased the levels of inflammatory cytokines (TNF-α, IL-6) and suppressed the activation of associated signaling pathways. In vitro, both Quercetin and Paeoniflorin reduced mast cell degranulation and the activation of TLR4 and PI3K-Akt pathways.</p><p><strong>Conclusion: </strong>This study, employing UPLC-Q-TOF-MS and both in vivo and in vitro experiments, provides a comprehensive analysis of the mechanism of DGYZ in CU. The findings indicate that DGYZ exerts therapeutic effects in CU by modulating immune responses. This research lays the foundation for a deeper understanding of its immunopharmacological mechanisms, potentially aiding the development of novel drugs and therapeutic strategies for CU management.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"81"},"PeriodicalIF":5.3,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12147246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257452","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}