Phytomedicine最新文献

{"title":"Corrigendum to \"β-Triketones from Leptospermum scoparium (mānuka) oil show potential as scabicides\" [Phytomedicine Volume 136, January 2025, 156321].","authors":"Nirupama A Nammunige, Kylie A Agnew-Francis, Deepani D Fernando, Sara Taylor, Hieng Lu, Sharon Chow, Gunter Hartel, Satomi Okano, Craig M Williams, Katja Fischer","doi":"10.1016/j.phymed.2025.157725","DOIUrl":"10.1016/j.phymed.2025.157725","url":null,"abstract":"","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":" ","pages":"157725"},"PeriodicalIF":8.3,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147459403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Ginsenoside Rg1 mitigates sepsis-associated acute respiratory distress syndrome by promoting autophagy through the Prdx1-PTEN/PI3K/AKT pathway\" [Phytomedicine Volume 154, May 2026, 158027].","authors":"Xiang Xue, Changbao Huang, Juan Chen, Weichao Ding, Yi Ren, Wei Zhang, Quan Li, Zhizhou Yang, Zhaorui Sun","doi":"10.1016/j.phymed.2026.158108","DOIUrl":"10.1016/j.phymed.2026.158108","url":null,"abstract":"","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":" ","pages":"158108"},"PeriodicalIF":8.3,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147616607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Harringtonine (HT) targets PARP-1 to inhibit TS mRNA m6A modification, blocks STAT3-induced miR-4521/TS axis and attenuates 5-fluorouracil (5-FU) resistance in NSCLC\" [Phytomedicine. 2025 Oct;146:157148].","authors":"Yu-Xi Qin, Yue-Ying Yang, Shi-Chen Zhang, Long-Tian Li, Ji-Fang Zhang, Ju-Bao Guo, Xin-Yang Li","doi":"10.1016/j.phymed.2026.158235","DOIUrl":"https://doi.org/10.1016/j.phymed.2026.158235","url":null,"abstract":"","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":" ","pages":"158235"},"PeriodicalIF":8.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147819805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quercetin alleviates liver injury in Wilson's disease by inhibiting ferroptosis","authors":"Chenling Zhao ,&nbsp;Guofang Yu ,&nbsp;Mengying Zhang ,&nbsp;Chunjing Liu ,&nbsp;Liwei Tian ,&nbsp;Lulu Tang ,&nbsp;An Zhou ,&nbsp;Wenming Yang ,&nbsp;Ting Dong","doi":"10.1016/j.phymed.2026.158155","DOIUrl":"10.1016/j.phymed.2026.158155","url":null,"abstract":"<div><h3>Background</h3><div>Wilson's disease (WD) is characterized by pathological copper accumulation, primarily driving liver injury. While ferroptosis is implicated in metal toxicity, its role in WD and the therapeutic potential of Quercetin (QUE) remain largely unexplored.</div></div><div><h3>Purpose</h3><div>This study aimed to systematically evaluate the therapeutic potential of QUE in a WD model and elucidate its underlying mechanisms, with a specific focus on the ferroptotic pathway.</div></div><div><h3>Methods</h3><div>The efficacy and mechanisms of QUE were investigated using both in vivo and in vitro WD models. Hepatic injury was assessed via histopathology, transmission electron microscopy, and serum biochemistry. Ferroptosis was evaluated by measuring iron content, lipid peroxidation, glutathione metabolism, reactive oxygen species, and mitochondrial membrane potential (using the JC-1 probe). Lipidomics analysis was employed to delineate QUE's impact on lipid metabolism. The central role of the ACSL4/LPCAT3/ALOX15 signaling pathway and QUE's intervention were validated through ACSL4 overexpression experiments, complemented by molecular docking, molecular dynamics simulations, cellular thermal shift assay, surface plasmon resonance, RT-qPCR, Western blotting, and immunofluorescence.</div></div><div><h3>Results</h3><div>QUE treatment significantly alleviated liver injury, iron overload, oxidative stress, lipid peroxidation, and mitochondrial dysfunction. Lipidomics revealed that QUE effectively reversed the aberrant accumulation of glycerolipids and restored glycerophospholipid metabolic homeostasis, indicating suppression of ferroptosis.. Mechanistically, QUE was confirmed to directly bind to ACSL4 and inhibit the ACSL4/LPCAT3/ALOX15 signaling pathway, thereby blocking ferroptosis.</div></div><div><h3>Conclusion</h3><div>QUE alleviates phospholipid peroxidation by inhibiting the ACSL4/LPCAT3/ALOX15 signaling pathway and exerts a multi-target effect against ferroptosis and liver injury by collaboratively remodeling iron homeostasis, restoring the antioxidant defense system, and protecting mitochondrial function.</div></div>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":"155 ","pages":"Article 158155"},"PeriodicalIF":8.3,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147658508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eicosapentaenoic acid attenuates heart failure with preserved ejection fraction via promoting TREM2-dependent efferocytosis","authors":"Yingying Xie ,&nbsp;Haoming He ,&nbsp;Yike Li ,&nbsp;Qiang Chen ,&nbsp;Sunjing Fu ,&nbsp;Zhe Wang ,&nbsp;Gaiyan Feng ,&nbsp;Yanping Li ,&nbsp;YanXiang Gao ,&nbsp;Jingang Zheng","doi":"10.1016/j.phymed.2026.157886","DOIUrl":"10.1016/j.phymed.2026.157886","url":null,"abstract":"<div><h3>Background</h3><div>Heart failure with preserved ejection fraction (HFpEF) constitutes over 50% of heart failure cases but lacks disease-modifying therapies. The pathophysiological role of eicosapentaenoic acid (EPA) in HFpEF remains undefined.</div></div><div><h3>Methods</h3><div>Integrated lipidomics was conducted across HFpEF discovery and validation cohorts. \"Two-hit\" murine HFpEF model combining high-fat diet (HFD) and 0.5 g/l-NAME​​ was established to recapitulate human metabolic-inflammatory pathology. EPA’s efficacy was evaluated through prophylactic/therapeutic interventions (160/320 mg/kg/day, human-equivalent 2/4 g/day). Mechanistic studies integrated transcriptomics, molecular docking, triggering receptor expressed on myeloid cells 2 (TREM2) knockout, and siRNA silencing.</div></div><div><h3>Results</h3><div>Plasma EPA deficiency correlated with diastolic dysfunction severity and conferred incremental diagnostic value. High-dose EPA (4 g/day equivalent) prevented/reversed diastolic impairment and apoptosis in HFpEF mice. EPA rescued impaired efferocytosis through dual modulation of TREM2, concurrently enhancing functional transmembrane receptor expression while suppressing pathological ectodomain shedding. TREM2 ablation attenuated EPA-mediated benefits on diastolic function and efferocytosis.</div></div><div><h3>Conclusion</h3><div>Our work identifies plasma EPA depletion as a potential biomarker for risk stratification and delineates the EPA-TREM2-efferocytosis axis as a putative therapeutic mechanism for HFpEF, suggesting the potential of EPA as a theranostic candidate.</div></div>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":"153 ","pages":"Article 157886"},"PeriodicalIF":8.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146143257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dingxin recipe Ⅲ ameliorates atherosclerosis through stard4-mediated regulation of hepatic lipid metabolism","authors":"Yuyan Gu ,&nbsp;Yao Jin ,&nbsp;Huashan Zhao ,&nbsp;Jingyu Tang ,&nbsp;Zhaoyong Li ,&nbsp;Saibo Cheng ,&nbsp;Yaxin Zhang ,&nbsp;Peikun He ,&nbsp;Zhouzhen Han ,&nbsp;Jieying He ,&nbsp;Fenghua Zhou ,&nbsp;Xiaoyu Liu ,&nbsp;Yuhua Jia","doi":"10.1016/j.phymed.2026.157924","DOIUrl":"10.1016/j.phymed.2026.157924","url":null,"abstract":"<div><h3>Background</h3><div>Atherosclerosis is the pathological basis of cardiovascular diseases. Dingxin Recipe III (DXRIII), a traditional Chinese herbal formula, has shown therapeutic effect for atherosclerosis, though its mechanisms remain unclear. This study aimed to investigate the effects and molecular mechanisms of DXRIII on atherosclerosis progression.</div></div><div><h3>Methods</h3><div>Male <em>ApoE^-/-</em> mice were fed a high-fat diet for 12 weeks to induce atherosclerosis, followed by 12 weeks of treatment with DXRIII (7.5 or 15 g/kg/d), atorvastatin, or saline. Serum lipids, liver enzymes, aortic plaques, and hepatic lipid deposition were assessed. Transcriptomics, proteomics, and metabolomics analyses identified hepatic molecular changes. Key targets were validated by western blot, RT-qPCR, immunohistochemistry, and hepatocyte models. Molecular docking and cellular thermal shift assay assessed the direct binding of DXRIII components to target proteins. Gene overexpression and knockdown experiments were conducted <em>in vitro</em> and <em>in vivo</em>.</div></div><div><h3>Results</h3><div>DXRIII significantly reduced aortic plaque areas, improved lipid profiles (decreased triglycerides, total cholesterol, and low-density lipoprotein-C), and alleviated hepatic steatosis. Integrated multi-omics revealed modulation of lipid metabolism pathways, including steroid hormone biosynthesis and arachidonic acid metabolism pathways. Steroidogenic acute regulatory-related lipid transfer protein 4 (Stard4) was identified as a key target, with expression positively correlated with gamma-linolenic acid and negatively correlated with corticosterone. Direct binding between DXRIII components and Stard4 was observed. <em>Stard4</em> overexpression reduced lipid accumulation, while knockdown aggravated lipid deposition and negated the effect of DXRIII. Hepatic <em>Stard4</em> knockdown aggravated atherosclerosis and lipid-related genes expression (<em>Angptl4, Apob, Soat2, Scarb1, Lepr</em>).</div></div><div><h3>Conclusion</h3><div>DXRIII attenuates atherosclerosis by upregulating hepatic Stard4 expression to restore lipid homeostasis and reduce lipid accumulation.</div></div>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":"153 ","pages":"Article 157924"},"PeriodicalIF":8.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146192383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resveratrol dual efficacy in high-altitude hypoxia and NAFLD: inhibits ferroptosis by modulating key proteins, including HIF-1α, ACSL4, and TfR1.","authors":"Minghui Zhao, Hongfang Mu, Qian Ji, Jiale Song, Fuyixuan Zheng, Tianlong Liu, Wenbin Li, Rong Wang","doi":"10.1016/j.phymed.2026.157992","DOIUrl":"10.1016/j.phymed.2026.157992","url":null,"abstract":"<p><strong>Background: </strong>The effects of persistent hypoxic conditions in high-altitude regions on metabolic disorders remain poorly understood and in-depth investigation into its underlying molecular mechanisms is notably insufficient. As a metabolism-associated liver disease, the pathogenesis of non-alcoholic fatty liver disease (NAFLD) under hypoxic conditions urgently requires clarification. Previous studies have demonstrated that resveratrol (Rsv) possesses significant anti-inflammatory, antioxidant, and lipid metabolism-modulating properties, and it can act as an inhibitor of ferroptosis. Yet its precise therapeutic efficacy and mechanism in hypoxic NAFLD remain to be further explored.</p><p><strong>Objective: </strong>This study aims to explore the potential mechanism by which Rsv improves the deterioration of NAFLD under hypoxia exposure.</p><p><strong>Methods: </strong>Herein, we performed concurrent interventions in both in vivo and in vitro models of NAFLD, comprehensively detecting biochemical indicators (inflammatory factors, oxidative stress markers, liver function), liver histopathological changes, and nucleic acid levels to assess the effects of Rsv. By introducing ferroptosis modulators, we measured core ferroptosis parameters (mitochondrial ultrastructure, Fe²⁺, 4-HNE, LPO levels, and key protein expressions) to define disease progression patterns. By HIF-1α silencing was employed to verify its regulatory roles in ferroptosis-related factors and NAFLD pathogenesis. Co-Immunoprecipitation assays and immunofluorescence co-localization were used to explore protein interactions among ACSL4, TfR1, and HIF-1α.</p><p><strong>Conclusion: </strong>Our results demonstrated that high-altitude hypoxia exacerbates NAFLD via inducing ferroptosis; HIF-1α upregulates the expression of key ferroptosis mediators (ACSL4, TfR1), and HIF-1α silencing attenuates ferroptosis. Rsv exerts therapeutic effects against hypoxia-related NAFLD by targeting the HIF-1α-mediated ferroptosis pathway. This study elucidates the pivotal role of HIF-1α-dependent ferroptosis in hypoxia-aggravated NAFLD, identifies the therapeutic targets and mechanisms of Rsv, and provides novel theoretical foundations and potential intervention strategies for clinical management of hypoxia-related NAFLD in high-altitude areas.</p>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":"153 ","pages":"157992"},"PeriodicalIF":8.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147318074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperoside as a promising multi-target candidate for neovascular age-related macular degeneration. mechanisms involving Wnt/β-catenin signaling, oxidative stress, and inflammation suppression.","authors":"Haoran Li, Yimin Xiong, Yanlin Zheng","doi":"10.1016/j.phymed.2026.157952","DOIUrl":"10.1016/j.phymed.2026.157952","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Neovascular age-related macular degeneration (nAMD), which is primarily characterized by choroidal neovascularization (CNV), encounters limitations with current therapeutic approaches, including treatment resistance and the burden of frequent injections, highlighting the need for exploring novel effective therapeutic agents and their mechanisms for nAMD management. Oxidative stress and inflammation are core pathogenic drivers of CNV in nAMD, and hyperoside (HYP)-a major flavonoid from Cuscuta chinensis, exhibits potent antioxidant and anti-inflammatory activities. These properties position HYP as a promising candidate for addressing the unmet treatment needs of nAMD and warrant further investigation into its mechanism of action in CNV modulation.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Purpose: &lt;/strong&gt;This study aimed to explore the therapeutic potential of HYP-the main active component of the traditional Chinese herb Cuscuta chinensis Lam., and to elucidate its underlying molecular mechanisms in treating nAMD.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Study design: &lt;/strong&gt;A combined in vivo and in vitro experimental strategy was adopted to systematically evaluate the therapeutic efficacy of HYP against nAMD and dissect the mechanistic basis of its action on CNV progression.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;This study adopted a multi-dimensional research approach: network pharmacology was first used to predict HYP's multi-target potential in regulating inflammation, oxidative stress, and vascular endothelial growth factor (VEGF) signaling; a murine model of laser-induced CNV was established to evaluate HYP's effects on CNV lesion area, retinal/choroidal damage, and inflammatory infiltration; reactive oxygen species (ROS) levels were detected, the expression of endogenous antioxidant enzymes (Cat, Nqo1, Sod2), Vegf, pro-inflammatory cytokines (Il-1β, Ccl2, Il-6, Tnf-α), and Wnt pathway-related genes (Myc, Plcb2, Rspo1, Wnt7a/7b, Ctnnb1) and protein (β-catenin); lipopolysaccharide (LPS)-stimulated ARPE-19 cells were used to corroborate HYP's antioxidant, anti-inflammatory effects, and Wnt pathway inhibition; molecular docking was employed to analyze the interaction between HYP and β-catenin; pharmacokinetic analysis was conducted to assess HYP's distribution in ocular tissues; and integrated transcriptomic analysis (RNA-seq) and Gene Expression Omnibus (GEO) database data analyses were performed to confirm the role of the Wnt pathway in human AMD and its correlation with intraocular inflammation.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Network pharmacology predicted that HYP has multi-target potential against inflammation, oxidative stress, and VEGF signaling; in the murine laser-induced CNV model, HYP treatment significantly reduced CNV lesion area, alleviated retinal/chorioretinal damage, and attenuated inflammatory infiltration; mechanistically, HYP effectively scavenged ROS, significantly upregulated the expression of endogenous antioxidant enzymes (Cat, Nqo1, Sod2), and","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":"153 ","pages":"157952"},"PeriodicalIF":8.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146259028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological targeting of NR4A1 restrains lipid metabolism–ferroptosis axis in UVR-induced skin aging","authors":"Hongjin Wang ,&nbsp;Jingjing Li ,&nbsp;Xiaogang Xu ,&nbsp;Yixi Zeng ,&nbsp;Guofeng Shi ,&nbsp;Lanyue Zhang ,&nbsp;Junxia Zheng ,&nbsp;Hui Li","doi":"10.1016/j.phymed.2026.157909","DOIUrl":"10.1016/j.phymed.2026.157909","url":null,"abstract":"<div><h3>Background</h3><div>Skin photo-aging induced by ultraviolet radiation (UVR) leads to aesthetic alterations, structural degradation, and loss of barrier function. Ferroptosis has been implicated upon UVR stress but the driving modifiers remain largely undefined. Naringin has been reported to exert protective effects against UVR damage, however, the underlying mechanisms remain incompletely understood.</div></div><div><h3>Purpose</h3><div>To explore the driving factors of UVR-induced ferroptosis and to comprehensively evaluate the effects and underlying mechanisms of naringin in repressing UVR-induced photo-aging.</div></div><div><h3>Methods</h3><div>A mouse model in which the dorsal skin, as well as a cell model using HaCaT keratinocytes, were exposed to UVR to simulate daily sun exposure. Lentivirus-mediated knockdown, ChIP-seq, and RNA-seq analysis were used to evaluate the role of NR4A1 in UVR-induced ferroptosis. RNA-seq and metabonomics were performed to elucidate the underlying mechanisms of naringin against photo-aging. Molecular dynamics simulations/DARTS/CETSA, and co-IP assays were employed to investigate the mechanism by which naringin regulates NR4A1 expression.</div></div><div><h3>Results</h3><div>Reduction of NR4A1 leads to excessive lipid metabolism and initiates ferroptosis in UVR-induced photo-aging. Naringin directly binds to NR4A1, enhancing its stability by preventing ubiquitin-mediated degradation, transcriptionally represses EGR1 and LDLR expression, thereby suppressing lipid peroxidation and ferroptotic damage. Remarkably, both genetic deficiency and pharmacological inhibition of NR4A1 across diverse models abolish the effects of naringin against photo-aging.</div></div><div><h3>Conclusion</h3><div>Our findings emphasize the critical role of NR4A1 in ferroptosis driven by dysregulated lipid metabolism and reveal the therapeutic potential of targeting NR4A1 with naringin in UVR-induced photo-aging, as well as in the other relevant lipid metabolism dysfunction disorders.</div></div>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":"153 ","pages":"Article 157909"},"PeriodicalIF":8.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of Jadwar (Delphinium denudatum Wall. ex Hook.f. & Thomson) in subclinical hypothyroid patients: A single-blind, randomized placebo controlled trial","authors":"Saduddin ,&nbsp;Mohd Aleemuddin Quamri ,&nbsp;Monalisha Samal ,&nbsp;Md Anzar Alam","doi":"10.1016/j.phymed.2026.157925","DOIUrl":"10.1016/j.phymed.2026.157925","url":null,"abstract":"<div><h3>Background and objectives</h3><div>Subclinical hypothyroidism (SCH) is a thyroid disorder characterized by the absence of prominent symptoms of thyroid deficiency. It is more prevalent in women (11.4%) than in men (6.2%). While levothyroxine is commonly used to treat SCH, its use remains a topic of debate. Therefore, this study aimed to assess the efficacy of <em>Jadwar</em> in managing subclinical hypothyroidism.</div></div><div><h3>Methods and materials</h3><div>A randomized, single-blind, single-center, placebo-controlled study was conducted at the National Institute of Unani Medicine, Bengaluru, between August 2022 and January 2023. A total of 30 subjects, aged 20–60 years, with elevated serum thyroid-stimulating hormone (TSH) levels (4.5-15 mIU/L), were enrolled and randomly assigned to either the test group (n=15) or the placebo group (n=15). Participants in the test group received 500 mg of <em>Jadwar</em>, while those in the placebo group were administered placebo capsules (starch powder), with both groups taking 1 g twice a day (4 × 500 mg) for 56 days. Serum TSH and free thyroxine (FT4) levels, along with safety parameters (serum blood urea, serum creatinine, aspartate aminotransferase, and alanine aminotransferase), were measured at baseline and at the end of the trial . Additionally, subjective symptoms (fatigue, constipation, weight gain, cold intolerance, and dry skin) were evaluated every two weeks throughout the trial period.</div></div><div><h3>Results</h3><div>The test group demonstrated significant improvement compared to the control group in subjective parameters, including fatigue and constipation, with p-values of &lt;0.001 and 0.028, respectively. However, no significant change was observed in weight gain (p=0.159). Additionally, a significant reduction in TSH levels was noted in the test group (p&lt;0.001) compared to the control group. Statistical analysis was performed using Student's t-test for hypothyroidism.</div></div><div><h3>Conclusion</h3><div>Treatment with <em>Jadwar</em> is effective for managing subclinical hypothyroidism (SCH) and demonstrates a good safety profile, with no adverse events reported.</div></div>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":"153 ","pages":"Article 157925"},"PeriodicalIF":8.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146181891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}