Phytotherapy Research最新文献

{"title":"Vitexin Alleviates Osteoarthritis Progression Through Sirtuin 3-Mediated Inhibition of Chondrocyte Ferroptosis and Mitochondrial Dysfunction.","authors":"Boyu Wu, Jiacong Xiao, Zhiqiang Luo, Zehua Chen, Gonghui Jian, Yifan Lu, Xiangling Ye, Yang Shu, Zhichao Tan, Liang Dong, Xiaolin Liao","doi":"10.1002/ptr.70410","DOIUrl":"10.1002/ptr.70410","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a prevalent degenerative joint disease in which ferroptosis and mitochondrial dysfunction contribute critically to disease progression, yet effective therapeutic strategies remain limited. Vitexin, a natural flavonoid with diverse pharmacological activities, has recently attracted attention for its potential protective effects against OA. This study investigated whether Vitexin alleviates OA progression through regulation of Sirtuin 3 (SIRT3)-mediated ferroptosis and mitochondrial dysfunction in chondrocytes. In vitro, erastin-induced rat chondrocytes were treated with Vitexin to evaluate ferroptosis, oxidative stress, and mitochondrial function. In vivo, a rat OA model was established to assess the protective effects of Vitexin on cartilage degeneration and subchondral bone destruction. Vitexin markedly reduced iron accumulation, lipid peroxidation, and reactive oxygen species generation while restoring mitochondrial function and redox homeostasis in chondrocytes. Moreover, Vitexin upregulated SIRT3, GPX4, and xCT expression, whereas SIRT3 knockdown partially abolished these protective effects. In vivo analyses further demonstrated that Vitexin attenuated cartilage degeneration, preserved subchondral bone architecture, and restored SIRT3 and GPX4 expression in OA rats. Collectively, these findings demonstrate that Vitexin alleviates OA progression through SIRT3-mediated inhibition of chondrocyte ferroptosis and mitochondrial dysfunction, highlighting its potential as a novel therapeutic strategy for OA.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"5551-5565"},"PeriodicalIF":8.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13549025/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148302736","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}

{"title":"Malvidin-3-O-Rhamnoside Alleviates Klebsiella pneumoniae -Induced Acute Lung Injury by Regulating Macrophage-Mediated Inflammatory and Oxidative Pathways.","authors":"Li Meng, Jing Chen, Baier Sun, Bo Yuan, Fei Jiang, Xueshuang Wang, Lulu Liang, Qingrong Li, Jian Feng, Xi Chen, Rongpeng Li","doi":"10.1002/ptr.70398","DOIUrl":"10.1002/ptr.70398","url":null,"abstract":"<p><p>Malvidin and its derivatives exhibit potent anti-inflammatory and antioxidant properties, yet their roles and mechanisms in infection-related acute lung injury (ALI) remain unclear. This study aimed to investigate the protective effects of malvidin-3-O-rhamnoside (Mv3rh) in Klebsiella pneumoniae (KP)-induced ALI and to elucidate the underlying mechanisms. A mouse model of KP-induced ALI was employed to assess the effects of Mv3rh on lung pathology, bacterial burden, myeloperoxidase (MPO) activity, alveolar macrophage proportion, cytokine levels, and survival. Mechanistic studies in alveolar macrophages included RNA sequencing, detection of reactive oxygen species (ROS), and evaluation of inflammasome activation, pyroptosis, and antioxidant responses using quantitative PCR (qPCR), Western blotting, flow cytometry, immunoprecipitation, and immunofluorescence. Potential interactions between Mv3rh with NOD-like receptor pyrin domain-containing 3 (NLRP3) or the Toll-like receptor 4/MD-2 complex were examined by molecular docking, cellular thermal shift assay (CETSA), and the interaction with TLR4 was further assessed by surface plasmon resonance (SPR). In vivo, Mv3rh pretreatment significantly mitigated KP-induced ALI, as evidenced by improved lung histopathology, reduced alveolar septal thickening, edema, and neutrophil infiltration, together with improved survival. These protective effects were accompanied by reduced systemic cytokine levels, lower bacterial burdens in the lung and blood, and partial restoration of alveolar macrophage-like cells in bronchoalveolar lavage fluid (BALF). In alveolar macrophages, Mv3rh suppressed TLR4/NF-κB signaling, reduced NLRP3 inflammasome priming and activation, inhibited cleavage of caspase-1 and GSDMD-N, and attenuated macrophage pyroptosis. In addition, Mv3rh activated the NRF2/HO-1 pathway, promoted NRF2 nuclear translocation, and restored antioxidant enzyme activities, including glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase (CAT). Mv3rh attenuates inflammation, oxidative stress, and macrophage pyroptosis in KP-induced ALI by regulating the TLR4/NF-κB/NLRP3 inflammasome axis and the NRF2/HO-1 antioxidant pathway. These findings suggest that Mv3rh possesses immunomodulatory activity and may be beneficial in KP-associated ALI.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"5420-5440"},"PeriodicalIF":8.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13549054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148252820","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}

{"title":"Trilobatin Ameliorates Myocardial Hypertrophy by Enhancing Mitophagy Through Activation of the Sentrin-Specific Protease 1/Sirtuin 3 Axis in Spontaneously Hypertensive Rats.","authors":"Ye-Li Li, Yi-Qi Li, Yun-Mei Luo, Yuan-Gui Liu, Jian-Mei Gao, Dan-Li Yang, Qi-Hai Gong","doi":"10.1002/ptr.70408","DOIUrl":"10.1002/ptr.70408","url":null,"abstract":"<p><p>Myocardial hypertrophy represents a maladaptive response in numerous cardiovascular disorders, and potentiating mitophagy has emerged as a potential therapy. Trilobatin (TLB) possesses multiple pharmacological properties, including the alleviation of cardiotoxicity. However, it remains uncertain whether TLB exerts anti-hypertrophic effects or, if so, by what mechanisms. This study was designed to determine whether TLB can attenuate hypertrophy and to elucidate the underlying pathways, focusing on mitophagy. We employed in vivo spontaneously hypertensive rats (SHR) and in vitro angiotensin II-stimulated cardiomyocytes to evaluate anti-hypertrophic effects. A comprehensive approach was employed, incorporating echocardiography, histological staining, transmission electron microscopy observations, and immunofluorescence to assess phenotypic changes. RNA sequencing, western blotting, immunofluorescence, and ELISA were utilized to elucidate the underlying mechanisms. Additionally, molecular docking, molecular dynamics simulations, and siRNA transfection techniques were applied to identify the target of TLB. The results showed that TLB markedly alleviated hypertrophy in SHR and inhibited angiotensin II-induced cardiomyocyte hypertrophy. Mechanistically, TLB enhanced mitophagy and reduced oxidative stress via activation of the sentrin-specific protease 1/sirtuin 3 (SENP1/SIRT3) axis, with direct binding to SENP1. Crucially, SENP1 knockdown abolished TLB's cardioprotective effects, confirming SENP1 as a pivotal mediator. Our findings indicate that TLB exerts anti-hypertrophic effects by promoting mitophagy and suppressing oxidative injury through the SENP1/SIRT3 axis, highlighting SENP1 as a promising therapeutic target for myocardial hypertrophy.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"5601-5614"},"PeriodicalIF":8.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13548929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148278527","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}

{"title":"Curcumol Inhibits the Laminin-Facilitated Malignant Progression in Small-Cell Lung Cancer via Disrupting Laminin-Integrin β1 Interaction.","authors":"Jing Qin, Huanhuan Huang, Mengzhen Xu, Lin Zhu, Haoli Liu, Xinyu Qian","doi":"10.1002/ptr.70411","DOIUrl":"10.1002/ptr.70411","url":null,"abstract":"<p><p>Laminin promotes tumor progression, but its role in small-cell lung cancer (SCLC) remains unclear. Curcumol, a natural compound from Curcumae Rhizoma, has anti-tumor activity. Here, we tested the hypothesis that Curcumol disrupts Laminin-Integrin β1 interaction to suppress SCLC. SBC-2 and H69 cells were cultured on Laminin-coated substrates. Cell functions were assessed by Transwell migration, colony formation, and MTT assays. Molecular mechanisms were investigated through qRT-PCR, Western blot, molecular docking, Co-IP, and Dot blot assays. Target specificity was confirmed by Integrin β1 mutagenesis. The therapeutic efficacy of Curcumol was evaluated in xenograft mouse models. Laminin enhanced malignant phenotypes in SCLC cells, accompanied by the activation of FAK/ERK and TGF-β/Smad2/3 pathways. Curcumol inhibited the laminin-promoted malignant phenotypes and epithelial-mesenchymal transition (EMT) in SCLC cells and suppressed the expression of related proteins. Mechanistic studies revealed that Curcumol directly bound to Integrin β1, competitively inhibiting the binding of Laminin to Integrin β1 and the activation of downstream signaling. Target specificity was validated through mutagenesis studies, where Curcumol exhibited reduced efficacy in Integrin β1-mutant cells. In vivo, Curcumol (100 mg/kg, oral) attenuated Laminin-driven tumor growth, suppressed EMT and FAK/ERK signaling, with no detectable toxicity. Integrin β1 is a key mediator of Laminin's pro-tumorigenic effects in SCLC. Curcumol disrupts Laminin-Integrin β1 interaction, inhibits FAK/ERK signaling and EMT, and suppresses tumor progression, representing a promising therapeutic strategy.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"5615-5633"},"PeriodicalIF":8.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13548952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148353113","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}

{"title":"Icaritin Sensitizes Hepatocellular Carcinoma to PD-L1 Therapy by NQO1-Dependent Ferroptosis Induction.","authors":"Zhen Li, Zimeng Shang, Zijing Xu, Donghao Yin, Jiahao Geng, Xiang Li, Jingwen Wang, Zhenzhen Ren, Meng Xu, Enxiang Zhang, Yanyu Xu, Guohao Wu, Zhenyu Zhu, Jiabo Wang, Xinhua Song","doi":"10.1002/ptr.70230","DOIUrl":"10.1002/ptr.70230","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) remains challenging with limited immunotherapy response. Despite its clinical promise in advanced HCC, the mechanisms of icaritin, especially concerning ferroptosis induction and immune modulation, remain elusive. This study aims to determine if the antitumor effect of icaritin involves the induction of ferroptosis via NAD(P)H quinone oxidoreductase 1 (NQO1) and if it can augment the efficacy of programmed cell death 1 ligand 1 (PD-L1) therapy by potentiating natural killer (NK) cell activity. Using human HCC cell lines (Huh7, Hep3B, PLC/PRF/5, SNU-449, and MHCC97-H) and two synergistic mouse models (Hepa1-6 and SgPten/c-Met), we examined icaritin's inhibition of tumor growth and induction of ferroptosis via the NQO1 pathway, monitoring key markers (reactive oxygen species [ROS], glutathione peroxidase 4 [GPX4], ferritin heavy chain 1 [FTH1]). The NQO1 inhibitor dicoumarol was employed to validate the pathway. Tumor microenvironment (TME) remodeling was assessed through cancer-associated fibroblasts (CAFs) markers and immune cell profiling, focusing on NK cell infiltration. Combination therapy with anti-PD-L1 was tested in vivo. Icaritin significantly inhibited HCC growth in vitro and in vivo. Its antitumor effect was mediated by NQO1-mediated ferroptosis, via elevated ROS, diminished mitochondrial membrane potential, and downregulated GPX4 and FTH1. Analysis of The Cancer Genome Atlas (TCGA) data revealed that NQO1 is overexpressed in human HCC tissues. Icaritin enhanced NK cell infiltration while reducing CAF abundance and suppressing recombinant focal adhesion kinase (FAK) and discoidin domain receptor 1 (DDR1) signaling. Notably, icaritin synergized with anti-PD-L1 therapy to enhance tumor suppression without increasing toxicity, correlating with potentiated NK cell immunity. Our findings demonstrate that icaritin triggered NQO1-mediated ferroptosis and remodeled TME to enhance NK cell recruitment and PD-L1 therapy efficacy. This provides rationale for evaluating icaritin-based combination immunotherapy in HCC through dual action on ferroptosis and NK cell activation.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"5339-5355"},"PeriodicalIF":8.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13548986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147434530","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}

{"title":"Correction to \"Shenlian Extract Decreases Mitochondrial Autophagy to Regulate Mitochondrial Function in Microvascular to Alleviate Coronary Artery No-Reflow\".","authors":"","doi":"10.1002/ptr.70399","DOIUrl":"10.1002/ptr.70399","url":null,"abstract":"","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"5581-5584"},"PeriodicalIF":8.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13549024/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318749","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}

{"title":"Protective Effects Induced by a Novel Food Supplement Based on Epilobium angustifolium, Ptychopetalum olacoides, Ginkgo biloba, and Equisetum arvense Extracts and Citrulline in the Lower Urinary Tract: Preclinical and Clinical Evidence.","authors":"Annalisa Chiavaroli, Alessandra Acquaviva, Simonetta Cristina Di Simone, Stefano Salvatore, Silvia Messina, Carolina Morgante, Chiara Lupi, Silvia Villa, Gokhan Zengin, Giustino Orlando, Luigi Menghini, Claudio Ferrante, Luigi Schips, Luca Cindolo, Michele Marchioni","doi":"10.1002/ptr.70438","DOIUrl":"https://doi.org/10.1002/ptr.70438","url":null,"abstract":"<p><p>Oxyfil is a dietary supplement including plant extracts from Epilobium angustifolium, Ptychopetalum olacoides (Muira puama), Ginkgo biloba, and Equisetum arvense and citrulline. The aim of the study was to investigate the protective effects on prostatic muscles of the Oxyfil formulation in an in vitro experimental model consisting of isolated mouse prostate specimens exposed to Escherichia coli lipopolysaccharide (LPS) as a pro-inflammatory stimulus. The study also assessed the tolerability and effectiveness of Oxyfil in alleviating lower urinary tract symptoms (LUTS) in patients with benign prostatic hyperplasia (BPH) when used in association with standard care. In the preclinical phase, Oxyfil was analysed via liquid chromatographic in order to identify and quantify phenolic compounds. Thereafter, the formulation was tested on isolated mouse prostate challenged with LPS in order to upregulate the gene expression of different pro-inflammatory and oxidative stress biomarkers, namely COX-2, i-NOS, TNFα, IL-6, VEGFA, HIF1α. The clinical trial was a retrospective, multicentre study. Fifty-nine patients were analyzed: 27 received Oxyfil, 18 Oxyfil + α-blocker, 7 Oxyfil + PDE5i, and 7 Oxyfil + 5-ARI. Key inclusion criteria were age 50-75 years, moderate to severe LUTS (IPSS), mild erectile dysfunction, and baseline Q_max 4-15 mL/s; exclusions were endocrine/hormonal erectile dysfunction, bladder-neck sclerosis, and urethral stricture. Treatment selection was non-randomized and left to the treating physician. The chromatographic analysis identified 25 phenolic compounds in the Oxyfil formulation. The total phenolic content can explain, albeit partially, the Oxyfil efficacy in blunting LPS-induced upregulation of the gene expression of all tested biomarkers in isolated prostate. The protective effects demonstrated in the preclinical phase also support, albeit partially, the clinical efficacy in ameliorating uroflowmetry and symptom outcomes in the patients' cohort. In conclusion, the present study demonstrated anti-inflammatory and antioxidant effects of the Oxyfil formulation in the prostate which corroborated the observed clinical outcomes.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148875419","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":"Correction to \"Oleoylethanolamide Ameliorates Motor Dysfunction Through PPARα-Mediates Oligodendrocyte Differentiation and White Matter Integrity After Ischemic Stroke\".","authors":"","doi":"10.1002/ptr.70393","DOIUrl":"10.1002/ptr.70393","url":null,"abstract":"","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"5356"},"PeriodicalIF":8.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13549008/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148164001","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}

{"title":"Apigenin Protects Hypertensive Intracerebral Hemorrhage by Regulating Trx1 Through Binding to PRDX2.","authors":"Hao-Chen Xu, Ming Liu, Ying-Ying Sun, Jie-Dan Ping, Qing-Hua Cui, Jing-Zhou Chen, Hao Li","doi":"10.1002/ptr.70439","DOIUrl":"https://doi.org/10.1002/ptr.70439","url":null,"abstract":"<p><p>Intracerebral hemorrhage (ICH) remains the most severe stroke subtype with high mortality and disability rates. Although apigenin has shown cerebroprotective potential in preclinical studies, its mechanism of action, particularly in hypertensive ICH, remains poorly understood. This study investigates the molecular pathway through which apigenin confers protection against hypertensive ICH. We employed a hypertensive ICH mouse model treated with varying apigenin doses. Through transcriptomic profiling, molecular docking, surface plasmon resonance (SPR), and pull-down assay, we identified peroxiredoxin 2 (PRDX2) as a direct target of apigenin. Prdx2^-/- mice and recombinant human thioredoxin 1 (rhTrx1) rescue experiments were utilized to validate the signaling pathway. Histological analysis, western blot, immunofluorescence, and zymography were applied to assess hemorrhage, oxidative stress, inflammation, and extracellular matrix (ECM) remodeling. Apigenin administration significantly reduced ICH incidence, hemorrhage volume, and area while enhancing vascular integrity, independent of blood pressure changes. We identified PRDX2 as a direct binding partner of apigenin, with their interaction stabilizing PRDX2 expression. PRDX2 deficiency abolished apigenin's protective effects and exacerbated oxidative stress, neuroinflammation, and vascular damage. Furthermore, apigenin upregulated Trx1 expression via PRDX2, and rhTrx1 administration rescued the protective phenotype in Prdx2^-/- mice by reducing oxidative damage, inflammatory cell infiltration, and vascular smooth muscle cell apoptosis. Our study elucidates a novel apigenin-PRDX2-Trx1 antioxidant signaling pathway that protects against hypertensive ICH through blood pressure-independent mechanisms. These findings not only provide a mechanistic foundation for developing apigenin-based therapeutics for cerebrovascular diseases, but also offer novel strategies and entry points for future clinical translation.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148866466","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":"Treatment of Nausea and Vomiting With Zingiber officinale in Pregnancy: An Umbrella Review of Systematic Reviews With Meta-Synthesis.","authors":"Zoya Tahergorabi, Mahdi Eslami, Morteza Arab-Zozani","doi":"10.1002/ptr.70405","DOIUrl":"10.1002/ptr.70405","url":null,"abstract":"<p><p>Affecting approximately 85% of expectant mothers during the first trimester, nausea and vomiting of pregnancy (NVP) are frequently reported symptoms. Despite numerous existing systematic reviews and meta-analyses (SRMs), findings remain inconsistent. Consequently, this study assesses the quality of these prior SRMs and investigates the efficacy of ginger as a treatment for NVP. A comprehensive search was conducted across PubMed, Scopus, Cochrane, and Web of Science from their inception through December 30, 2024. This review includes peer-reviewed English-language SRMs investigating ginger as a therapeutic intervention for pregnancy-related nausea and vomiting. Methodological rigor was evaluated using the AMSTAR-2 checklist, while evidence quality was assessed via the GRADE approach. Findings are synthesized narratively through content analysis. The study protocol was prospectively registered in the PROSPERO database. This study analyzed 18 systematic reviews, of which eight (44%) incorporated meta-analyses. The Rhodes Index of Nausea and Vomiting (RINV) emerged as the primary tool for evaluating outcomes. Regarding study reporting and transparency, seven studies registered their protocols in PROSPERO, while eight adhered to the PRISMA checklist. Overall, the included reviews demonstrated low methodological quality, with a mean score of 11.77. Specifically, 28% (n = 5) were rated as high quality, 28% (n = 5) as moderate, 22% (n = 4) as low, and 22% (n = 4) as critically low. Taking ginger supplements (usually between 450 and 1950 mg daily) significantly decreases the severity and occurrence of nausea and vomiting compared to a placebo. This benefit is more noticeable for nausea than for vomiting, where the results are less consistent. Numerous studies have shown that ginger does not raise the risk of adverse effects, such as spontaneous abortion or side effects like heartburn and drowsiness, when compared to a placebo or vitamin B6. Current evidence clearly shows that ginger is a safe and effective treatment for nausea and vomiting during pregnancy, with effectiveness similar to vitamin B6 and some traditional medications, and it has a good safety profile. Ginger can be recommended as a dependable medicinal herb for women dealing with NVP, though more research is needed to determine the best doses and confirm long-term safety.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":"5538-5550"},"PeriodicalIF":8.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13549022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148284063","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}