Phytotherapy Research最新文献

{"title":"Mechanism of Cucurbitacin B Targeting ZNF70/NLRP3 Axis Against Inflammation-Associated Colorectal Cancer.","authors":"Shen Cao, Yi Tai, Yuhan Wang, Jing Han, Ming Yue Li, Young Joon Surh, Yue Xing, Hong Xiang Zuo, Xuejun Jin, Juan Ma","doi":"10.1002/ptr.70329","DOIUrl":"https://doi.org/10.1002/ptr.70329","url":null,"abstract":"<p><p>Cucurbitacin B is a naturally occurring tetracyclic triterpenoid extracted from plants in the Cucumis melo L. It demonstrates various pharmacological activities, such as hepatoprotective, anti-inflammatory, and anti-tumor effects. However, its therapeutic effect on inflammation-associated colorectal cancer (CRC) and its mechanism of action have not been elucidated. This study is aimed to investigate the effects of cucurbitacin B on inflammation-associated CRC and the mechanism of action. In vitro, the effect of cucurbitacin B on the inflammatory response and the related ZNF70/NLRP3 pathway was examined using western blotting, CCK-8, ELISA, and immunofluorescence assays. In the HCT116/THP-1 supernatant co-culture system, EdU, colony formation, and wound healing assays were performed to evaluate the effects of cucurbitacin B on the proliferation, migration, and epithelial-mesenchymal transition (EMT) progression of HCT116 cells in response to inflammation. In vivo, a mouse model of inflammatory CRC was constructed by administering azoxymethane (AOM) and dextran sodium sulfate (DSS). To study the role of ZNF70, an adenoviral vector AAV was used to knock out ZNF70 in mice. High-performance liquid chromatography (HPLC) was utilized to assess the toxic impact of cucurbitacin B on mice. Our results indicate that cucurbitacin B reduces the expression of NLRP3 inflammasome-associated proteins by downregulating the production of ZNF70. The co-culture experiment showed that cucurbitacin B inhibited the proliferation, migration, and EMT of HCT116 cells in the inflammatory microenvironment. In vivo studies demonstrated that the knockdown of ZNF70 restored body weight, improved colon length, reduced tumor burden, and increased survival rate in AOM/DSS model mice. This effect was further enhanced by the addition of cucurbitacin B. The HPLC results showed that cucurbitacin B was non-toxic to the heart, liver, spleen, lungs, and kidneys of mice. In conclusion, the downregulation of ZNF70 by cucurbitacin B inhibits the activation of NLRP3 inflammasomes and reduces the promoting effect of the inflammatory microenvironment on CRC proliferation, migration, and the EMT process. Our findings may provide new insights for the development of treatments for inflammation-associated CRC.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856969","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}

{"title":"Fisetin Promotes Autophagy in Osteosarcoma by Activating the ROS/FOXO3 Axis via Oxidative Stress.","authors":"Yujie Hu, Lanyi Wei, Jingjing Meng, Danfeng Xiang, Xiangqi Zhang, Jingxian Zhang, Quanjun Yang, Yangyun Zhou, Lingyan Xu, Mengyue Wang, Junjun Chen, Yonglong Han","doi":"10.1002/ptr.70347","DOIUrl":"https://doi.org/10.1002/ptr.70347","url":null,"abstract":"<p><p>Osteosarcoma is a malignant bone tumor that occurs in adolescents and for which surgical resection and chemotherapy are the treatments of first choice. However, tumor cell metastasis and the toxic effects of chemotherapeutic agents bring great challenges to the treatment of osteosarcoma. Fisetin, a dietary flavonoid derived from vegetables and fruits, plays a therapeutic role in many cancers, but its role and underlying mechanism on osteosarcoma remain unrevealed. This study found that fisetin significantly inhibited the proliferation of osteosarcoma cells and organoids. RNA sequencing revealed that forkhead box O3 (FOXO3) may be a key target of fisetin in its anti-osteosarcoma activity, which was also verified by immunofluorescence. siFOXO3 reversed the effects of fisetin on proliferation, apoptosis, and migration of osteosarcoma cells. Fisetin exerts its effects by targeting the ROS/FOXO3 pathway to promote the binding of FOXO3 to the microtubule-associated protein light chain 3 (LC3) promoter, thereby upregulating LC3 levels and inducing autophagy. Subsequently, activated autophagy further triggers ferroptosis, while silencing LC3 reversed fisetin-induced ferroptosis. In vivo, fisetin inhibited tumor growth while promoting FOXO3 and LC3, and inhibiting SLC7A11 protein expression. Therefore, fisetin-induced autophagy in osteosarcoma cells may be associated with the reactive oxygen species (ROS)/FOXO3 axis, thereby promoting ferroptosis. These findings highlight fisetin's potential as a unique therapy for osteosarcoma.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147841610","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}

{"title":"Efficacy and Safety of Melaleuca alternifolia (Tea Tree) Oil for Acne-A Systematic Review and Meta-Analysis.","authors":"Yixin Ye, Jun Jie Lim, Zongxun Huang, Fook Tim Chew","doi":"10.1002/ptr.70344","DOIUrl":"https://doi.org/10.1002/ptr.70344","url":null,"abstract":"<p><p>Acne vulgaris is a common chronic inflammatory skin disorder that begins in adolescents and often persists into adulthood, with substantial psychosocial impact. Tea tree oil (TTO) has been explored as a topical treatment for acne, but clinical evidence for its efficacy and safety remain limited and inconsistent. This systematic review and meta-analysis synthesizes available clinical data to evaluate TTO's therapeutic effects and safety profile in acne management. PubMed, Embase, and Web of Science were systematically searched for clinical studies published up to August 2025 that evaluated TTO for acne treatment. Study selection, data extraction, and risk-of-bias assessment were independently conducted by trained reviewers. Pooled estimates were calculated using fixed- or random-effects models according to heterogeneity, quantified using the I² statistic. Seven studies comprising 445 patients were included. The use of TTO was associated with a reduction in acne severity compared with control groups (pooled odds ratio [pOR] = 0.74, 95% confidence intervals [CI]: 0.63-0.88). Adverse events were predominantly local and mild. An exploratory pooled analysis indicated a lower incidence of mild itching with TTO compared to the corresponding control treatments in the included studies (pOR = 0.09, 95% CI: 0.03-0.23), with similar trends observed for dryness, burning sensation, erythema, and scaling. Publication bias was not evident based on Egger's test and the trim-and-fill analysis, and overall risk of bias was assessed as low. Current evidence suggests that TTO is associated with a modest reduction in acne severity and generally acceptable short-term tolerability. Larger, high-quality trials with standardized formulations and long-term follow-up are needed to define its clinical role.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147841590","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}

{"title":"Gentiopicroside Ameliorates Psoriasis-Like Dermatitis by Modulating Immune Homeostasis and Suppressing NF-κB Activation.","authors":"Lingyun Du, Xiaoke Zhao, Jingjing Wei, Shanrong Lv, Mingming Li, Yi Leng, Kemei Yu, Qingqing Xu, Chunhong Zhang","doi":"10.1002/ptr.70342","DOIUrl":"https://doi.org/10.1002/ptr.70342","url":null,"abstract":"<p><p>Psoriasis is a common chronic immune-mediated inflammatory skin disease that presents significant challenges in clinical management. Gentiopicroside (GPS), a bioactive compound derived from Gentiana scabra, has been reported to possess anti-inflammatory and immunomodulatory properties. However, its potential role in the treatment of psoriasis remains unclear. This study aimed to investigate the therapeutic effects of GPS on psoriasis-like dermatitis and elucidate its underlying mechanisms. A psoriasis-like dermatitis model was established in BALB/c mice using imiquimod (IMQ). The therapeutic efficacy of GPS was evaluated based on clinical and histopathological improvements. Flow cytometry was used to analyze immune cell populations in the spleen and peripheral blood. In vitro, the effects of GPS on bone marrow-derived dendritic cells (BMDCs) were assessed in an inflammatory model. RNA sequencing was performed to identify differentially expressed genes and key signaling pathways in BMDCs after GPS treatment. Molecular docking was employed to predict the binding affinity between GPS and potential targets, which were further validated using Western blotting and immunofluorescence. GPS treatment significantly alleviated psoriasis-like skin lesions in IMQ-induced mice, improving both clinical manifestations and histopathological alterations. GPS reduced the proportions of lymphocytes and dendritic cells and attenuated Th17-driven inflammation, thereby contributing to a more balanced immune milieu. In vitro, GPS inhibited the maturation and activation of BMDCs. Transcriptomic profiling demonstrated that GPS modulated multiple immune- and cytokine-associated pathways, particularly the NF-κB signaling pathway. Molecular docking suggested a strong binding affinity between GPS and NF-κB p65, while Western blotting and immunofluorescence confirmed that GPS suppressed phosphorylated NF-κB p65 nuclear translocation. GPS exerts anti-psoriatic effects through multimodal mechanisms, including immunomodulation and suppression of NF-κB activation. These findings provide experimental evidence and a theoretical basis for the development of GPS as a potential therapeutic agent for psoriasis.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147841621","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}

{"title":"Naturally Occurring Coumarins as Promising Antimicrobial Agents: Latest Progress.","authors":"Geni Gako, Ramesh Joga, Annapurna Padaraju, Sravani Yerram, Sandeep Kumar, Gautam Kumar","doi":"10.1002/ptr.70365","DOIUrl":"https://doi.org/10.1002/ptr.70365","url":null,"abstract":"<p><p>One of the twenty-first century's most significant threats to human health is the rise of microbial diseases. Infectious diseases are caused mainly by microorganisms, including bacteria, viruses, fungi, and protozoa. These organisms are responsible for significant increases in morbidity and mortality worldwide. Since the discovery of penicillin, antibiotics have been used to treat microbial illnesses. Antibiotic abuse and overuse in humans, animals, and plants, as well as in the treatment of non-microbial disorders, have led to the fast development of multidrug-resistant and high-virulence pathogens in recent decades. Microbes with greater pathogenicity and virulence have emerged due to antibiotic resistance. Most antibiotics remain ineffective in treating resistant pathogens and require high doses or combination therapy to overcome antimicrobial resistance. Since most synthetic antimicrobials have acquired resistance, natural products (NPs) offer more effective alternatives to overcome the resistance and can sensitize the microbes to antibiotics. Coumarin-based scaffolds possess several pharmacological properties, including antimicrobial, antiviral, antiprotozoal, and antiparasitic activities. Notably, most coumarins exhibit antimicrobial activity through distinct pathways from conventional antibiotics; thus, they can help address antibiotic resistance and effectively treat human infections. This review discusses the recently identified natural coumarins, their antibacterial, antiviral, antifungal, and antiprotozoal activities, their action as efflux pumps and as biofilm inhibitors, and their formulations as potential means to combat microbial infections. We also provide detailed coverage of the coumarin-based patents and the gain of market exclusivity. The discussed natural coumarin-based compounds could be promising agents for treating microbial diseases.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147841567","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}

{"title":"Scutellarin Alleviates Hepatic Steatosis by Autophagy-Mediated NCoR1/PPARα-Driven Fatty Acid β-Oxidation and Enhancing Peroxisome Biogenesis.","authors":"Jianmei Zheng, Lu Cheng, Yingmin Wei, Mingshi Ren, Lei Wang, Jingwen Wang, Wuliu Zhou, Hui Huang, Feihua Wu","doi":"10.1002/ptr.70367","DOIUrl":"https://doi.org/10.1002/ptr.70367","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent chronic liver disorder with limited treatment and manifests as hepatic lipid accumulation. The reduction of nuclear receptor corepressor 1 (NCoR1) activates the nuclear receptor PPARα, which plays a crucial role in alleviating lipid accumulation. We found that Scutellarin (Scu) regulated autophagy-mediated NCoR1/PPARα to enhance fatty acid (FA) β-oxidation and peroxisome production, thereby alleviating the lipid accumulation of MASLD. We used palmitic acid (PA)-treated human hepatocellular carcinoma (HepG2) and alpha mouse liver 12 (AML12) cells, as well as high-fat diet-fed C57BL/6J mice to evaluate the protective effect of Scu on MASLD. Scu reduced the levels of total cholesterol, triglycerides, and lipid droplets, whereas it dose-dependently increased the levels of β-hydroxybutyrate. In addition, Scu increased mRNA and protein expression of PPARα and promoted the transcriptional activity of FA β-oxidation-related target genes. In vitro, inhibition of PPARα with small interfering RNA (siRNA) abolished the activation of FA β-oxidation by Scu. Cellular thermal shift assay and drug affinity responsive target stability demonstrated that Scu did not interact directly with PPARα. Moreover, Scu increased the protein expression of 70-kDa peroxisomal membrane protein and the mRNA expression of peroxisome biogenesis-related genes. These effects were reversed by PPARα-siRNA. Scu improved the impaired autophagy while reducing the mRNA and protein expression of NCoR1. Notably, Scu reduced the colocalization of NCoR1 with PPARα and increased its colocalization with the autophagosome GABARAP. 3-MA, an autophagy inhibitor, attenuated Scu-mediated protective effects by FA β-oxidation and peroxisome biogenesis both in vitro and in vivo. In summary, Scu reduces lipid accumulation by improving the impaired autophagy, decreasing NCoR1 expression to activate PPARα, thereby simultaneously enhancing FA β-oxidation and peroxisome biogenesis, ultimately ameliorating hepatic steatosis.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147841570","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}

{"title":"The TRIM27/STING Axis Mediates Schisandrin B-Induced Inhibition of Myeloid-Derived Suppressor Cells Accumulation to Potentiate Anti-PD-1 Immunotherapy in Hepatocellular Carcinoma.","authors":"Lei Huang, Siying Li, Ziqing Li, Zhuo Qin, Yanan Sun, Caifang Qin, Chunmei Wang, He Li, Jinghui Sun, Jiping Wu, Zhihong Zhang","doi":"10.1002/ptr.70368","DOIUrl":"https://doi.org/10.1002/ptr.70368","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is characterized by a highly immunosuppressive microenvironment, which contributes to its unfavorable clinical outcomes. Myeloid-derived suppressor cells (MDSCs) play a crucial role in this process. Schisandrin B (SchB) shows anti-tumor potential, but its mechanism in suppressing MDSCs remains unclear. This study investigates how SchB inhibits MDSCs accumulation and enhances anti-PD-1 therapy efficacy in HCC.SchB's efficacy and mechanism were investigated both in vitro and in vivo. In vitro, MTT, wound healing, EdU, colony formation, flow cytometry, ELISA, western blot, immunofluorescence, Co-IP, molecular dynamics (MD), and CETSA assays were employed to evaluate the therapeutic effects and mechanistic action of SchB on HCC. In vivo, a mouse HCC xenograft model was used to evaluate whether SchB could enhance the anti-tumor effect of PD-1 mAb and the potential mechanism.Mechanistically, SchB suppressed TRIM27 expression, disrupted the interaction between TRIM27 and STING, and enhanced STING/TBK1/IRF3 signaling, thereby suppressing the secretion of IL-6 and GM-CSF as well as the accumulation of MDSCs. SchB could directly bind to TRIM27 and downregulate its expression, thereby enhancing STING protein stability. In vivo, SchB effectively reduced MDSCs accumulation while promoting T cell recruitment, thereby augmenting the antitumor efficacy of PD-1 mAb therapy.SchB up-regulates STING by suppressing TRIM27, inhibits IL-6/GM-CSF secretion, and reduces MDSCs accumulation, indicating that SchB has the potential to be a promising candidate for PD-1 inhibitor therapy in HCC.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147841619","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}

{"title":"Anti-Allergic Potential of Chamaecrista nomame and Its Compound Luteolin for Novel Asthma Therapy.","authors":"Tae Kyeom Kang, Myungsuk Kim, Tam Thi Le, Geon Park, Yuna Jung, Hyobin Jeong, Youngsang Yoo, Wook-Bin Lee, Sang Hoon Jung","doi":"10.1002/ptr.70363","DOIUrl":"https://doi.org/10.1002/ptr.70363","url":null,"abstract":"<p><p>Asthma is a chronic inflammatory disease driven by dysregulated immune responses and mast cell activation. While corticosteroids remain the primary treatment, their long-term use is associated with adverse effects, necessitating safer alternatives. This study aims to evaluate the therapeutic potential and underlying mechanisms of Chamaecrista nomame (CN) extract and its active compound luteolin in allergic asthma. We performed bioactivity-guided fractionation to identify active compounds from CN extract. An ovalbumin-induced murine asthma model was utilized to investigate the efficacy of CN in vivo. Transcriptomic analysis of bone marrow-derived mast cells was conducted to elucidate molecular pathways regulated by luteolin. Additionally, cytokine release assays were performed using house dust mite-stimulated human peripheral blood mononuclear cells (PBMCs). CN extract demonstrated potent anti-allergic effects by significantly inhibiting mast cell degranulation and inflammatory mediator release. Luteolin was identified as the primary active compound, modulating FcεRI-mediated signaling in mast cells. In the murine asthma model, CN markedly reduced airway inflammation, mucus hypersecretion, and immune cell infiltration, with efficacy comparable to corticosteroids. Transcriptomic data indicated that luteolin suppresses proinflammatory cytokine production by downregulating NF-κB and MAPK signaling pathways. Moreover, CN and luteolin significantly inhibited cytokine release from house dust mite-stimulated human PBMCs, highlighting clinical relevance. These findings suggest that CN and luteolin may serve as promising natural therapeutic agents for allergic asthma, offering a potential alternative to conventional treatments.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147841616","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}

{"title":"Astragaloside IV Enhances Mitophagy to Alleviate Renal Ischemia/Reperfusion Injury via PINK1/Parkin Pathway.","authors":"Lin Liu, Zonghui Xu, Shujing Wu, Man Li, Ruoan Wei, Mpofu Uphakeme Inobubele Sitholumusa, Junqiu Liu, Guoyin Kai","doi":"10.1002/ptr.70369","DOIUrl":"https://doi.org/10.1002/ptr.70369","url":null,"abstract":"<p><p>Astragaloside IV (AS-IV), a primary bioactive component of Astragalus membranaceus (AM). It is very effective in regulating renal diseases. However, the possible underlying mechanism of AS-IV on renoprotection remains unclear. The aim of this study is to find out the regulation mechanism of AS-IV on ischemia/reperfusion injury-induced Acute kidney injury (IRI-AKI). At first, AS-IV was confirmed to significantly alleviate renal dysfunction, inflammation, and renal tubular epithelial cell apoptosis in IRI-AKI mice. Then, it was found that AS-IV alleviated mitochondrial dysfunction and renal tubular epithelial cell injury induced by IRI. Growing evidence has suggested that PINK1/Parkin-mediated mitophagy plays a critical protective role in IRI. Based on this, we hypothesized that AS-IV might exert renoprotective effects through activating the PINK1/Parkin mitophagy pathway. After 3-MA inhibition of autophagy, AS-IV no longer showed its protective effect on HK-2 cells in a hypoxic environment. Through further molecular docking, cell thermal migration, and gene targeted silencing experiments, we confirmed that AS-IV activates the PINK1/Parkin mitophagy pathway and ultimately alleviates IRI-AKI. In summary, all these comprehensive experimental findings indicated that AS-IV can be used as a functional food for the prevention of renal ischemia/reperfusion injury.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147841596","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}

{"title":"Curcumin Alleviates Bone Cancer Pain by Inhibiting Satellite Glial Cell Activity via Janus Kinase 1/Signal Transducer and Transcription 3 Pathway Activator.","authors":"Xinchao Jiang, Yi Song, Mei Fang, Xin Wang, Biao Zhang, Haiyong Li, Jianxue Qian","doi":"10.1002/ptr.70366","DOIUrl":"https://doi.org/10.1002/ptr.70366","url":null,"abstract":"<p><p>Curcumin is the main active component of Curcuma longa L and has anti-inflammatory, antitumor, and neuroprotective properties, making it a potential candidate for bone cancer pain management. Network pharmacology, molecular docking, and molecular dynamics simulations were used to screen and validate core therapeutic targets of curcumin in bone cancer pain. An in vivo mouse model of bone cancer pain was established via intrafemoral injection of Lewis lung cancer cells. A series of in vivo assays was conducted to evaluate pain sensitivity, bone microstructure, inflammatory cytokines, pain-related neuropeptides, and protein expression levels. In silico analysis verified that curcumin has a strong binding affinity for JAK1 and STAT3. In vivo results demonstrated that curcumin dose-dependently elevated the paw withdrawal threshold and latency, as well as ameliorated bone mineral density and bone destruction. Curcumin also suppressed pro-inflammatory cytokines, substance P, calcitonin gene-related peptides, and inhibited satellite glial cell activation by blocking the JAK1/STAT3 pathway. Notably, JAK1 agonist (RO8191) co-administration markedly reversed the analgesic effects of curcumin. Curcumin targets the JAK1/STAT3 signaling pathway, inhibits satellite glial cell activation, downregulates pro-inflammatory cytokine release, and pain-related neuropeptide expression. Therefore, curcumin exerted a significant analgesic effect against bone cancer pain. Elucidating the analgesic mechanism revealed the core therapeutic targets of curcumin in treating bone cancer pain. This study provides experimental evidence for further research on bone cancer pain.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147841564","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}