Phytotherapy Research最新文献_第4页

Salvianolic Acid B Inhibits ZBP1-Mediated PANoptosis in Mycobacterium tuberculosis-Infected Macrophages by Targeting TNFR1. 丹酚酸B通过靶向TNFR1抑制zbp1介导的结核分枝杆菌感染巨噬细胞PANoptosis

IF 6.3 2区医学

Phytotherapy Research Pub Date : 2025-09-01 Epub Date: 2025-07-27 DOI: 10.1002/ptr.70042

Jingjing Shen, Yan Fu, Fanglin Liu, Jianchao Wu, Hemin Zhang, Jinxia Sun, Zhulei Miao, Xin Jiang

{"title":"Salvianolic Acid B Inhibits ZBP1-Mediated PANoptosis in Mycobacterium tuberculosis-Infected Macrophages by Targeting TNFR1.","authors":"Jingjing Shen, Yan Fu, Fanglin Liu, Jianchao Wu, Hemin Zhang, Jinxia Sun, Zhulei Miao, Xin Jiang","doi":"10.1002/ptr.70042","DOIUrl":"10.1002/ptr.70042","url":null,"abstract":"The increasing rates of drug resistance in Mycobacterium tuberculosis (Mtb) have made controlling tuberculosis more challenging. Excessive programmed cell death helps mediate Mtb transmission. Salvianolic acid B (Sal B), a water-soluble extract of Salvia miltiorrhiza, has been reported to inhibit programmed cell death and excessive inflammation. This study aimed to investigate the potential inhibitory mechanism of Sal B on PANoptosis. The inhibitory effect of Sal B on PANoptosis was evaluated by western blotting, ELISA, and other techniques in an in vitro model of Mtb H37Ra-infected macrophages. The roles of ZBP1 and TNFR1 in PANoptosis were explored by small interfering RNA transfection. In addition, the inhibitory effect of Sal B on PANoptosis and the hyperinflammatory response was verified by western blotting, hematoxylin and eosin staining, and immunohistochemistry in an in vivo model of inflammatory injury in the lungs of LPS-infected mice. Sal B inhibited the protein levels of key molecules of Mtb-mediated PANoptosis and hindered the assembly of the PANoptosome consisting of ASC, ZBP1, RIPK1, RIPK3, and Caspase 8. Sal B may further inhibit PANoptosis by binding to TNFR1 and suppressing ZBP1 levels. In addition, the results of in vivo studies verified that Sal B could ameliorate LPS-induced pathological injury in mouse lung tissues. Sal B can target TNFR1 to achieve a regulatory effect on macrophage PANoptosis. This provides new ideas for Sal B as a host-directed therapy drug to attenuate the excessive inflammatory response induced by Mtb infection.","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"4028-4045"},"PeriodicalIF":6.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144732728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Luteolin Treats Obese Rats With Polycystic Ovary Syndrome by Improving Liver Lipid Metabolism and Regulating the Gut Microbiota. 木犀草素通过改善肝脏脂质代谢和调节肠道微生物群治疗肥胖大鼠多囊卵巢综合征。

IF 6.3 2区医学

Phytotherapy Research Pub Date : 2025-09-01 Epub Date: 2025-08-06 DOI: 10.1002/ptr.70043

Guoyu Dai, Yin Zhang, Cong Shen, Yang Jiao, Wen Shen, Fan Yu, Ruoshuang Liu, Dong Wang, Guoyue Yuan, Jue Jia

{"title":"Luteolin Treats Obese Rats With Polycystic Ovary Syndrome by Improving Liver Lipid Metabolism and Regulating the Gut Microbiota.","authors":"Guoyu Dai, Yin Zhang, Cong Shen, Yang Jiao, Wen Shen, Fan Yu, Ruoshuang Liu, Dong Wang, Guoyue Yuan, Jue Jia","doi":"10.1002/ptr.70043","DOIUrl":"10.1002/ptr.70043","url":null,"abstract":"Polycystic ovary syndrome (PCOS) and obesity share a bidirectional relationship. While previous studies have indicated the anti-obesity effects of luteolin, its role in PCOS exacerbated by obesity remains unclear. This study aimed to investigate the ameliorative effects of luteolin on obese rats with PCOS and explore its underlying mechanisms. We established a rat model of PCOS with obesity and administered luteolin to evaluate its mitigating effects on the metabolic phenotype. Liver transcriptomics and fecal metagenomics were employed to analyze potential targets and alterations in the gut microbiota composition associated with luteolin's effects. Results showed that luteolin reduced body weight, improved estrous cycles, polycystic ovarian morphology, and glucose tolerance, and lowered serum levels of triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-c) in the model rats. Importantly, luteolin significantly alleviated hepatic steatosis and reversed the expression of 138 key differentially expressed genes (DEGs) in the liver, including UQCRC2, IRS2, NFIX, and ALDH6A1. In addition, luteolin significantly increased the alpha diversity of the gut microbiota and modulated its composition, specifically increasing the relative abundance of Bacteroidota and decreasing that of Firmicutes. Our findings suggest that luteolin exerts beneficial effects on PCOS with obesity, potentially mediated through the improvement of hepatic lipid metabolism and the restoration of gut microbiota homeostasis. Luteolin emerges as a promising therapeutic candidate for managing PCOS with obesity.","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"4171-4180"},"PeriodicalIF":6.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144789713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Coptisine Improves Liver Inflammation in Sepsis by Regulating STAT1/IRF1/GPX4 Signaling-Mediated Kupffer Cells Ferroptosis. 黄柏碱通过调节STAT1/IRF1/GPX4信号介导的Kupffer细胞凋亡改善脓毒症中的肝脏炎症

IF 6.3 2区医学

Phytotherapy Research Pub Date : 2025-09-01 Epub Date: 2025-08-12 DOI: 10.1002/ptr.70063

Bingwen Zhu, Chang Sun, Dongrong Luo, Yuying Liang, Aolin Jiang, Zehui Jiang, Haihua Luo, Gang Yuan, Chenyang Huang, Shaoqing Liu, Lei Li, Yong Jiang

{"title":"Coptisine Improves Liver Inflammation in Sepsis by Regulating STAT1/IRF1/GPX4 Signaling-Mediated Kupffer Cells Ferroptosis.","authors":"Bingwen Zhu, Chang Sun, Dongrong Luo, Yuying Liang, Aolin Jiang, Zehui Jiang, Haihua Luo, Gang Yuan, Chenyang Huang, Shaoqing Liu, Lei Li, Yong Jiang","doi":"10.1002/ptr.70063","DOIUrl":"10.1002/ptr.70063","url":null,"abstract":"Sepsis is a life-threatening condition characterized by organ dysfunction, with the liver being particularly vulnerable due to inflammation triggered by Kupffer cell activation. Ferroptosis, an iron-dependent form of regulated cell death associated with macrophages, has emerged as a key pathogenic mechanism. This study aimed to investigate the protective effects of coptisine (COP), a natural alkaloid, against sepsis-induced hepatic ferroptosis and injury using in vivo and in vitro models. Sepsis was induced in mice via cecal ligation and puncture (CLP) or lipopolysaccharide (LPS) challenge, followed by treatment with COP, ferrostatin-1 (Fer-1, a ferroptosis inhibitor), or 2-NP. In vitro, Kupffer cells were stimulated with LPS + IFN-γ and erastin to induce inflammation and ferroptosis, then treated with COP or Fer-1. Multiple techniques were employed, including histopathology, enzyme-linked immunosorbent assay (ELISA), quantitative PCR (qPCR), Western Blot, immunofluorescence (IF), molecular docking, bio-layer interferometry (BLI), and cellular thermal shift assay (CETSA), to evaluate the STAT1/IRF1/GPX4 signaling axis. Additionally, serum markers from sepsis patients were analyzed. In septic mice, COP significantly attenuated liver injury, inflammation, and ferroptosis. In Kupffer cells, COP suppressed erastin-induced ferroptosis. Mechanistically, COP directly bound to STAT1, inhibiting its phosphorylation and subsequent IRF1 activation, while restoring GPX4 expression. Overexpression of STAT1 abolished the protective effects of COP. Clinical data revealed elevated p-STAT1 and IRF1 levels alongside reduced GPX4 in sepsis patients. COP exerts hepatoprotective effects in sepsis by inhibiting ferroptosis through the STAT1/IRF1/GPX4 pathway, highlighting its potential as a therapeutic agent for sepsis-associated liver injury.","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"4308-4326"},"PeriodicalIF":6.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144822272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Association of Total Flavonoid and Flavonoid Subclass Intake With Cancer-Related and All-Cause Mortality Among Cancer Patients. 总黄酮和总黄酮亚类摄入与癌症患者全因死亡率的关系

IF 6.3 2区医学

Phytotherapy Research Pub Date : 2025-09-01 Epub Date: 2025-08-03 DOI: 10.1002/ptr.70058

Yi-Jie Jia, Xiao-Min Li, Fei-Hong Hu, Meng-Wei Ge, Lu-Ting Shen, Xiao-Peng Xia, Hong-Lin Chen

{"title":"Association of Total Flavonoid and Flavonoid Subclass Intake With Cancer-Related and All-Cause Mortality Among Cancer Patients.","authors":"Yi-Jie Jia, Xiao-Min Li, Fei-Hong Hu, Meng-Wei Ge, Lu-Ting Shen, Xiao-Peng Xia, Hong-Lin Chen","doi":"10.1002/ptr.70058","DOIUrl":"10.1002/ptr.70058","url":null,"abstract":"Flavonoids remain controversial regarding their role in cancer-related mortality and all-cause mortality in cancer patients. A comprehensive search was conducted on Web of Science, PubMed, and CINAHL up to February 2024. Using adjusted hazard ratios (HRs), we compared flavonoid intake in the highest with lowest categories. Random-effects models were employed when the I2 statistic surpassed 50%, while fixed-effects models were utilized otherwise. Fifteen eligible articles, comprising 19 cohorts, met the inclusion criteria. A significant inverse association was observed between total flavonoid intake and all-cause mortality (HR: 0.95, 95% CI: 0.91-0.99). However, the study found no significant association between total flavonoid intake and reduced cancer-related mortality risk (HR: 0.93, 95% CI: 0.83-1.04). A meta-regression analysis showed that the hazard ratio significantly decreased with the duration of follow-up (p = 0.005). Among flavonoid subclasses, flavan-3-ols intake was linked to a reduced risk of cancer-related mortality (HR: 0.74, 95% CI: 0.59-0.94). The consumption of flavanones, flavones, and isoflavones was correlated with a reduced likelihood of mortality from any cause, with summary HRs of 0.97 (95% CI: 0.95-0.99), 0.95 (95% CI: 0.92-0.98), and 0.88 (95% CI: 0.80-0.97), respectively. This study indicated that dietary intake of total flavonoids, flavanones, flavones, and isoflavones is inversely correlated with the risk of all-cause mortality in cancer patients.","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"4126-4140"},"PeriodicalIF":6.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144776051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Potential Therapeutic Actions of Flavonoids Present in Propolis That Modulate Vascular Endothelial Growth Factor Signaling to Regulate Angiogenesis. 蜂胶中黄酮类化合物调节血管内皮生长因子信号调节血管生成的潜在治疗作用。

IF 6.3 2区医学

Phytotherapy Research Pub Date : 2025-09-01 Epub Date: 2025-08-09 DOI: 10.1002/ptr.70029

Yipeng Lin, Janney Z Wang, Yihe Niu, Ling Zhu, Rujee K Duke, Colin C Duke, Michael Murray, Fanfan Zhou

{"title":"Potential Therapeutic Actions of Flavonoids Present in Propolis That Modulate Vascular Endothelial Growth Factor Signaling to Regulate Angiogenesis.","authors":"Yipeng Lin, Janney Z Wang, Yihe Niu, Ling Zhu, Rujee K Duke, Colin C Duke, Michael Murray, Fanfan Zhou","doi":"10.1002/ptr.70029","DOIUrl":"10.1002/ptr.70029","url":null,"abstract":"Propolis is a plant-derived substance collected by honeybees that has a range of potential therapeutic applications. Propolis consists of resins, waxes, and fatty acids, as well as essential oils and other organic compounds. The pharmacologically active components of propolis include phenols and flavonoids, among others. Flavonoids that are found in propolis include chrysin, quercetin, galangin, kaempferol, and apigenin. Angiogenesis is the growth of new blood vessels from endothelial cell precursors. Angiogenesis is important in normal physiology and development. Pathological angiogenesis is widely implicated in human diseases, such as retinal diseases, cancers, and inflammatory diseases; currently, many of these conditions lack effective treatments. The process of angiogenesis is modulated by pro-angiogenic factors, in particular, Vascular Endothelial Growth Factor (VEGF). Flavonoids, including several that are present in propolis, have been found to inhibit angiogenesis by attenuating VEGF signaling. Although promising, such findings are primarily based on preclinical studies, and few clinical studies have evaluated the efficacy and toxicity of flavonoids in vivo. This review outlines the therapeutic potential of essential flavonoids from propolis that may have value as anti-angiogenic agents by modulating VEGF signaling. Overall, the findings suggest that flavonoids that are present in propolis are potential agents for the treatment of human diseases in which pathological angiogenesis is activated.","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"4230-4246"},"PeriodicalIF":6.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12423498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144804479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MicroRNAs for Diabetes Management: From Natural Bioactive Compounds to Nucleotide Networks. 用于糖尿病管理的microrna：从天然生物活性化合物到核苷酸网络。

IF 6.3 2区医学

Phytotherapy Research Pub Date : 2025-09-01 DOI: 10.1002/ptr.70084

Junren Chen, Maozhu Luo, Siqi Qin, Cheng Peng, Dan Li

{"title":"MicroRNAs for Diabetes Management: From Natural Bioactive Compounds to Nucleotide Networks.","authors":"Junren Chen, Maozhu Luo, Siqi Qin, Cheng Peng, Dan Li","doi":"10.1002/ptr.70084","DOIUrl":"https://doi.org/10.1002/ptr.70084","url":null,"abstract":"MicroRNAs (miRNAs) have emerged as critical regulators in the pathogenesis of diabetes mellitus (DM) and its associated complications via orchestrating key cellular processes. Natural bioactive components such as flavonoids, polysaccharides, saponins, alkaloids, terpenoids, as well as anthraquinones derived from berries, herbs, vegetables, and fishes have been extensively demonstrated to treat or prevent DM and related complications through targeting miRNAs-mediated signaling pathways. Mechanistically, these compounds treat/prevent DM and its complications principally by modulating processes including glucose homeostasis, inflammatory response, oxidative stress, apoptosis, and autophagy, neovascularization, and fibrosis. This paper reviews the roles of miRNAs in DM and relevant complications and focuses on the potential molecular mechanisms of natural bioactive compounds in the treatment of DM and its complications by targeting miRNAs, with the aim of facilitating the development of miRNA-targeted edible natural products as functional foods as well as their clinical application in the treatment of DM and related complications.","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144965031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

l-Theanine Improves Learning and Memory Through Attenuation of NOX4-Mediated Ferroptosis in Hippocampal Neurons of Sleep-Deprived Mice. l-茶氨酸通过抑制睡眠剥夺小鼠海马神经元nox4介导的铁下垂改善学习和记忆。

IF 6.3 2区医学

Phytotherapy Research Pub Date : 2025-09-01 Epub Date: 2025-07-19 DOI: 10.1002/ptr.70048

Xuanxuan Huang, Xinglong Lu, Zhenghua Wu, Hongfei Wu, Zhongwen Xie, Yin Cao

{"title":"l-Theanine Improves Learning and Memory Through Attenuation of NOX4-Mediated Ferroptosis in Hippocampal Neurons of Sleep-Deprived Mice.","authors":"Xuanxuan Huang, Xinglong Lu, Zhenghua Wu, Hongfei Wu, Zhongwen Xie, Yin Cao","doi":"10.1002/ptr.70048","DOIUrl":"10.1002/ptr.70048","url":null,"abstract":"Sleep deprivation (SD) can negatively affect the central nervous system owing to its detrimental effects on learning and memory. l-theanine, known for its antioxidative properties, can confer neuroprotection by enhancing learning and memory. Here, we explored whether l-theanine could improve learning and memory by inhibiting the NOX4-mediated ferroptosis in hippocampal neurons caused by SD. The Morris water maze (MWM) was employed to assess learning and memory ability. MDA, SOD, GSH, LDH, and Fe2+ levels were measured using their specific assay kits. The degree of damage in hippocampal neurons was examined by Nissl staining. The process of ferroptosis in the hippocampus of SD mice and HT22 cells was analyzed using transmission electron microscopy (TEM), immunohistochemistry, flow cytometry, and Western blotting assays. l-Theanine treatment significantly increased the frequency of mice crossing the platform. Moreover, it conferred protection on hippocampal neurons and mitochondria in SD mice. Furthermore, l-theanine mitigated Erastin-induced oxidative stress and ferroptosis in HT22 cells. In addition, it reversed the abnormal expression of proteins including PSD-95, SYN, NOX4, TFRC, ACSL4, Nrf2, Keap1, SLC7A11, P53, HO-1, NQO1, FTH1, and GPX4 in the hippocampus of SD mice and in the HT22 cells induced by Erastin. Moreover, the neuroprotection of l-theanine was reversed by the GLX351322 agent. l-Theanine treatment inhibited hippocampal ferroptosis by attenuating NOX4, suggesting that it can be used to mitigate the adverse effects of SD.","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"3952-3965"},"PeriodicalIF":6.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

4'-Hydroxychalcone Induces Ferroptosis in Glioblastoma Through the xCT/GSH/GPX4 Axis Under the Regulation of the AKT/mTORC1/4EBP1 Pathway. 在AKT/mTORC1/4EBP1通路的调控下，4′-羟基查尔酮通过xCT/GSH/GPX4轴诱导胶质母细胞瘤铁凋亡

IF 6.3 2区医学

Phytotherapy Research Pub Date : 2025-09-01 Epub Date: 2025-08-25 DOI: 10.1002/ptr.70004

Renshuang Zhao, Yaru Li, Yunyun Liu, Xia Yang, Hongyang Li, Changzheng Wu, Zhehao Zhao, Yan Yan, Zirui Liu, Shanzhi Li, Yiquan Li

{"title":"4'-Hydroxychalcone Induces Ferroptosis in Glioblastoma Through the xCT/GSH/GPX4 Axis Under the Regulation of the AKT/mTORC1/4EBP1 Pathway.","authors":"Renshuang Zhao, Yaru Li, Yunyun Liu, Xia Yang, Hongyang Li, Changzheng Wu, Zhehao Zhao, Yan Yan, Zirui Liu, Shanzhi Li, Yiquan Li","doi":"10.1002/ptr.70004","DOIUrl":"10.1002/ptr.70004","url":null,"abstract":"Glioblastoma multiforme (GBM) is a common and malignant tumor in the field of neurosurgery. Natural chemotherapeutic agents are an appealing option due to their diverse activities and low cost. Ferroptosis, a form of programmed cell death, holds great potential for treating resistant cancers. The specific mechanism by which 4'-hydroxychalcone extracted from Glycyrrhiza glabra L. induces glioma cell death remains unclear. This study aims to explore the molecular mechanism of 4'-hydroxychalcone's effect on glioma cells. Through CCK-8 assay, cell scratch and invasion assay, q-PCR technology, WB detection and immunofluorescence, the inhibitory effect of 4'-hydroxychalcone on glioma and its mechanism were analyzed. The study found that 20 μM 4'-hydroxychalcone could induce ferroptosis and inhibit the proliferation and epithelial-mesenchymal transition of glioma cells. Subsequent analysis revealed that this process of ferroptosis was triggered through the xCT/GSH/GPX4 axis, which was regulated by the AKT/mTORC1/4EBP1 pathway. Similar tumor inhibitory effects to the clinical drug temozolomide were also observed in the in vivo tumor model. Long-term animal toxicity experiments showed that high doses of 4'-hydroxychalcone (100 mg/kg) did not cause damage to the organs of the animals. This study provides new insights into tumor ferroptosis research and traditional Chinese medicine-based treatment of GBM.","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"4348-4365"},"PeriodicalIF":6.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144964990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reniformin A Suppresses Triple-Negative Breast Cancer Progression by Inducing DRP1-Mediated Mitochondrial Dysfunction and Apoptosis. Reniformin A通过诱导drp1介导的线粒体功能障碍和细胞凋亡抑制三阴性乳腺癌进展。

IF 6.3 2区医学

Phytotherapy Research Pub Date : 2025-09-01 Epub Date: 2025-07-27 DOI: 10.1002/ptr.70034

Yifei Guan, Lei Liu, Wei Wang, Ran Zheng, Pinghao Lin, Yalin Liu, Siyu Chen, Huiyu Zhu, Xinhui Liu, Hua Huang

{"title":"Reniformin A Suppresses Triple-Negative Breast Cancer Progression by Inducing DRP1-Mediated Mitochondrial Dysfunction and Apoptosis.","authors":"Yifei Guan, Lei Liu, Wei Wang, Ran Zheng, Pinghao Lin, Yalin Liu, Siyu Chen, Huiyu Zhu, Xinhui Liu, Hua Huang","doi":"10.1002/ptr.70034","DOIUrl":"10.1002/ptr.70034","url":null,"abstract":"Reniformin A (RA) is a natural compound extracted from the medicinal herb Isodon excisoides, known for its tumor-suppressive properties in lung cancer. Yet, its effects and mechanisms of action in other cancers, such as triple-negative breast cancer (TNBC), remain unclear. This study aims to investigate the potential effects and underlying molecular mechanisms of RA in TNBC. Here, we demonstrate the significant anti-cancer activity of RA against TNBC, primarily through the induction of mitochondrial dysfunction and intrinsic apoptosis. Molecular docking and in vitro validation revealed that RA interacts directly with DRP1 at two primary binding sites. This interaction promotes the association of DRP1 with BAX, facilitating their translocation to mitochondria, where they trigger mitochondrial permeabilization, leading to the release of cytochrome c and subsequent apoptosis. Additionally, DRP1 is essential for RA-induced apoptosis; disruption of the RA-DRP1 interaction not only impeded the mitochondrial translocation of DRP1 and BAX but also significantly reduced RA's impact on mitochondrial function, apoptosis, and TNBC progression. The inhibition of the RA-DRP1 interaction also compromised the activation of apoptosis and diminished the effectiveness of RA as a chemotherapeutic agent in vivo. Collectively, these findings suggest that Reniformin A significantly inhibits TNBC by inducing DRP1/BAX-mediated apoptosis, offering a promising therapeutic strategy for TNBC treatment.","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"4011-4027"},"PeriodicalIF":6.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144732727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Berberine Ameliorates Atrial Remodeling and Inhibits the Atrial Fibrillation of Mice via Regulating NLRP3 Inflammasome. 小檗碱通过调节NLRP3炎性体改善小鼠心房重构和抑制心房颤动。

IF 6.3 2区医学

Phytotherapy Research Pub Date : 2025-09-01 Epub Date: 2025-07-26 DOI: 10.1002/ptr.70011

Na An, Fan Yang, Nian Liu, Yonghong Gao, Hongcai Shang, Yanwei Xing

{"title":"Berberine Ameliorates Atrial Remodeling and Inhibits the Atrial Fibrillation of Mice via Regulating NLRP3 Inflammasome.","authors":"Na An, Fan Yang, Nian Liu, Yonghong Gao, Hongcai Shang, Yanwei Xing","doi":"10.1002/ptr.70011","DOIUrl":"10.1002/ptr.70011","url":null,"abstract":"Increased cardiomyocyte-specific activation of the NLRP3 inflammasome contributes to the development of atrial fibrillation (AF). Berberine (BBR) exhibits numerous beneficial effects on the cardiovascular system. This study investigated how the NLRP3 inflammasome regulates susceptibility to hypertension-induced AF and the effects of BBR on this susceptibility. Blood pressure was monitored in mice using a tail pressure sensor device. AF was induced by burst stimulation of the esophagus. The target proteins of BBR were screened by network pharmacology, and molecular docking was performed. The changes in atrial tissue structure were observed by pathological tissue staining and transmission electron microscopy. Western blot analysis was used for protein verification. Intracellular Ca2+ release was detected by confocal laser microscopy and the IonOptix system. We found that in angiotensin II (Ang II)-induced AF, NLRP3 inflammasome activation was inhibited, ultimately inhibiting hypertensive AF susceptibility. In a recombinant adeno-associated virus 9 (rAAV9)-NLRP3 overexpression model, BBR mitigated the increase in systolic blood pressure and the development and progression of AF by inhibiting the NLRP3 inflammasome. This study provides hitherto undocumented evidence that the NLRP3 inflammasome acts as a critical regulator in the progression of Ang II-induced AF and that BBR may serve as a viable treatment for AF by inhibiting NLRP3.","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"3998-4010"},"PeriodicalIF":6.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144732692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0