Phytomedicine最新文献

{"title":"Comparative and Pan-Chloroplast Genome Reveals Molecular Markers, High Haplotype Diversity, and Geographic Structure in Medicinal Leymus Species (Triticeae, Poaceae).","authors":"Yanze Zhang, Zhuo Yuan, Lingyi Lyu, Zhibin Xu, Bo Feng, Qiang Zhou, Xiaoli Fan, Tao Wang","doi":"10.1016/j.phymed.2026.158595","DOIUrl":"10.1016/j.phymed.2026.158595","url":null,"abstract":"<p><strong>Background: </strong>The genus Leymus includes traditional medicinal species. A lack of comprehensive chloroplast genome analyses, coupled with morphological similarities, has impeded advances in Leymus species identification, molecular evolution, and phylogeny. Qinghai Province, the primary habitat of L. secalinus, requires characterization of its chloroplast genome variation for elucidating adaptive mechanisms.</p><p><strong>Purpose: </strong>To elucidate the phylogenetic relationships and genomic features of Leymus chloroplasts, as well as the adaptive variation of Leymus secalinus populations in Qinghai Province.</p><p><strong>Methods: </strong>Chloroplast genomes of 28 Leymus secalinus and 2 Leymus flexus individuals from Qinghai were de novo sequenced and analyzed alongside 36 public accessions. Comparative genomic analyses revealed features and evolutionary patterns. We also constructed a L. secalinus pan-plastome atlas for genomic diversity analysis.</p><p><strong>Result: </strong>Leymus chloroplast genomes exhibit a typical Poaceae quadripartite structure and lack ycf1, ycf2, and accD genes. Sequence variation is mainly concentrated in intergenic spacer regions, while coding regions are highly conserved. Phylogenetic analyses indicate that L. secalinus is most closely related to L. flexus. Highly variable regions (petA and trnL-UAA intron) partially resolve phylogenetic relationships, suggesting their potential utility as supplementary DNA barcodes for species identification. Pan-plastome analyses reveal weak phylogeographic structure across saline-alkaline habitats, suggesting that historical dispersal and lineage admixture have played a dominant role in shaping current chloroplast haplotype distributions.</p><p><strong>Conclusion: </strong>Comparative analyses of Leymus chloroplast genomes provide insights into genome evolution and phylogenetic relationships. Pan-plastome analysis further indicates a highly conserved chloroplast genomic background across environmentally heterogeneous populations of L. secalinus.</p>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":"159 ","pages":"158595"},"PeriodicalIF":11.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148562824","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":"Natural polysaccharides as multi-target therapeutic candidates for Alzheimer's disease: Mechanisms, structure-activity relationships, and translational perspectives.","authors":"Shiyan Luo, Jiafu Guo, Jiayi Xu, Juxian Song, Yuan Dai, Shijun Xu","doi":"10.1016/j.phymed.2026.158585","DOIUrl":"10.1016/j.phymed.2026.158585","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is increasingly recognized as a systems-level disorder involving amyloid-β (Aβ) deposition, tau pathology, oxidative stress, mitochondrial dysfunction, neuroinflammation, synaptic impairment, and microbiota-gut-brain axis dysregulation. Although previous reviews have summarized the anti-AD effects of natural polysaccharides according to individual pathological pathways, an integrated framework linking polysaccharide structure, gut microbial metabolism, peripheral immune regulation, and central AD pathology remains insufficiently developed.</p><p><strong>Purpose: </strong>This review aims to provide an updated and integrative synthesis of natural polysaccharides as multi-target therapeutic candidates for AD, with particular emphasis on their mechanistic networks, structure-activity relationships, and translational potential.</p><p><strong>Methods: </strong>A systematic PubMed search was performed for studies published from January 1, 2016, to June 7, 2026. Eligible studies investigated natural polysaccharides as primary therapeutic interventions in in vivo AD models. Reviews, editorials, purely in vitro studies, studies using polysaccharides solely as drug-delivery carriers, synthetic derivatives, and inseparable compound formulations were excluded. Seventy-four original studies were included for mechanistic and structure-activity analyses.</p><p><strong>Results: </strong>Natural polysaccharides were found to regulate multiple interconnected AD-related processes, including Aβ production, aggregation, and clearance, tau phosphorylation, redox homeostasis, glial activation, inflammasome signaling, synaptic plasticity, cholinergic function, intestinal barrier integrity, gut microbiota composition, and short-chain fatty acid production. Unlike earlier pathway-based summaries, this review proposes a structure-microbiota-metabolite-barrier-inflammation-redox-brain pathology framework to explain how polysaccharide structural features may determine microbial utilization, metabolite generation, immune modulation, and downstream neuroprotective effects.</p><p><strong>Conclusion: </strong>Natural polysaccharides represent promising multi-target candidates for AD prevention and treatment. Future studies should prioritize structurally defined polysaccharide fractions, causal microbiota validation, pharmacokinetic/pharmacodynamic profiling, biomarker-guided assessment, and rigorously designed clinical trials.</p>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":"159 ","pages":"158585"},"PeriodicalIF":11.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148579904","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 \"Diosgenin as a substitute for cholesterol alleviates NAFLD by affecting CYP7A1 and NPC1L1-related pathway\" [Phytomedicine, 125 (2024), 155299].","authors":"Mengyao Yan, Shuli Man, Yujie Dai, Yixin Zhao, Long Ma, Wenyuan Gao","doi":"10.1016/j.phymed.2026.158605","DOIUrl":"10.1016/j.phymed.2026.158605","url":null,"abstract":"","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":" ","pages":"158605"},"PeriodicalIF":11.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148606781","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 \"Liquiritigenin targets transferrin receptor to potentiate ferroptosis sensitivity in colorectal cancer cells\" [Phytomedicine. 154 (2026) 158057].","authors":"Rui Li, Chen Song, Tiantian Jia, Tao Xia, Mengmeng Guo, Qi Wang, Yuan Yao, Xin Xu, Xunxia Bao, Peng Yang, Zongwei Li","doi":"10.1016/j.phymed.2026.158416","DOIUrl":"10.1016/j.phymed.2026.158416","url":null,"abstract":"","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":" ","pages":"158416"},"PeriodicalIF":11.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148353308","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 \"Bushentongluo formula counteracts BMSCs senescence to alleviate postmenopausal osteoporosis by activating mitophagy via the SENP1-SIRT3 pathway\" [Phytomedicine 152 (2026) 157827].","authors":"Shuai Chen, Lingling Yu, Ningsheng Tian, Qilong Zhao, Miaochao Qin, Liansheng Shao, Pengfei Sun, Peng Ma, Junwu Wang, Penghua Fang, Wen Min","doi":"10.1016/j.phymed.2026.158500","DOIUrl":"10.1016/j.phymed.2026.158500","url":null,"abstract":"","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":" ","pages":"158500"},"PeriodicalIF":11.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148376371","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 \"Quercetin attenuates chondrocyte anoikis via modulation of mesenchymal stromal cell-derived small extracellular vesicles to promote cartilage repair in osteoarthritis\" [Phytomedicine 146 (2025) 157146].","authors":"Feng Cheng, Haotian Hua, Yiwen Zhu, Yangming Zhu, Pengqiang Lou, Peijian Tong, Yang Zhang","doi":"10.1016/j.phymed.2026.158501","DOIUrl":"10.1016/j.phymed.2026.158501","url":null,"abstract":"","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":" ","pages":"158501"},"PeriodicalIF":11.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148387933","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":"Huaier induces lipophagy to promote ferroptosis and chemosensitivity via de-acetylation of PLIN3 in triple-negative breast cancer.","authors":"Tingting Ma, Tong Niu, Yaming Li, Qifeng Yang","doi":"10.1016/j.phymed.2026.158559","DOIUrl":"10.1016/j.phymed.2026.158559","url":null,"abstract":"<p><strong>Background: </strong>Huaier, a traditional Chinese medicinal mushroom, has been shown to have anti-tumor properties in our previous studies. However, its role and underlying mechanisms in regulating doxorubicin (DOX) sensitivity in triple-negative breast cancer (TNBC) remain unclear.</p><p><strong>Purpose: </strong>This study investigated whether Huaier could potentiate TNBC cell susceptibility to DOX and explored the associated molecular mechanisms involving lipophagy and ferroptosis.</p><p><strong>Methods: </strong>The therapeutic potential of Huaier in combination with DOX was evaluated using in vitro cell viability and colony formation assays and validated in xenograft models in vivo. Ferroptosis and lipophagy were characterized by quantifying ROS, MDA, and GSH, as well as by staining with BODIPY and Lyso-Tracker. Underlying mechanisms were dissected using acetylation spectrum profiling, LC-MS, co-immunoprecipitation (co-IP), and proximity ligation assays (PLA).</p><p><strong>Results: </strong>Huaier significantly enhances TNBC cell sensitivity to DOX both in vitro and in vivo by triggering lipophagy and ferroptosis. Acetylation spectrum profiling revealed that Huaier selectively deacetylates Perilipin 3 (PLIN3) at lysine 65 (K65), which was responsible for Huaier's regulatory effects on TNBC lipophagy, ferroptosis, and DOX sensitivity. Mechanistically, Huaier upregulated histone deacetylase 3 (HDAC3) to de-acetylate PLIN3 at K65. Our data also showed that deacetylation of PLIN3 at K65 increased PLIN3-mediated recruitment of ATG16L1, promoting lipophagy and ferroptosis, and ultimately improving chemo-sensitivity in TNBC cells.</p><p><strong>Conclusion: </strong>This study showed that Huaier enhanced DOX sensitivity by deacetylating PLIN3 and subsequently induction of lipophagy and ferroptosis. These results indicate that Huaier may serve as a promising adjuvant therapeutic approach to augment chemotherapy efficacy in TNBC.</p>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":"159 ","pages":"158559"},"PeriodicalIF":11.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148497999","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":"Dihydroartemisinin promotes ABCG5/G8-mediated cholesterol efflux to potentiate anti-PD-1 therapy through YAP1-TEAD1 complex disruption in hepatocellular carcinoma.","authors":"Yuting Gao, Yi Gong, Zhimin Du, Wei Zhang, Lin Lai, Meiqi Lan, Zhuoyue Jia, Xiaoyong Song, Yajun Xiong, Yanli Gong, Yanguang Yang, Xinli Shi","doi":"10.1016/j.phymed.2026.158584","DOIUrl":"10.1016/j.phymed.2026.158584","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Cholesterol accumulation influences the efficacy of immune checkpoint inhibitors (ICIs) in hepatocellular carcinoma (HCC), highlighting a targetable metabolic vulnerability. Dihydroartemisinin (DHA) has shown antitumor activity in HCC; however, its role in regulating cholesterol accumulation remains unclear.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Purpose: &lt;/strong&gt;The purpose of this study is to explore whether DHA enhances anti-PD-1 immunotherapy in HCC by promoting cholesterol efflux and to elucidate the underlying molecular mechanism.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A Hepa1-6 subcutaneous tumor-bearing mouse model was established to assess the combined effect of DHA and anti-PD-1 treatment. Multiplex immunohistochemistry was performed to evaluate cytotoxic T-cell infiltration and activation in the tumor microenvironment (TME). Patient-derived organoids (PDOs) were established to evaluate the antitumor activity of DHA. The regulatory mechanism of YAP1/TEAD1 on ABCG5/G8 transcription was explored using chromatin immunoprecipitation (ChIP) qPCR, dual-luciferase reporter assays, and functional gain/loss experiments. DEN/TCPOBOP-induced primary liver tumor model with hepatocyte-specific Yap1 deletion was used to assess the effect of YAP1 deficiency on cholesterol efflux. The direct effect of DHA on the YAP1-TEAD1 interaction was assessed through co-immunoprecipitation (Co-IP) and immunofluorescence (IF) co-localization, and surface plasmon resonance (SPR) analysis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;DHA significantly potentiates anti-PD-1 therapy in HCC-bearing mice, accompanied by reduced serum and intratumoral total cholesterol (TC) levels and increased CD8/granzyme B double-positive signals in tumor tissues, without significant body weight loss. In parallel, ABCG5/G8-mediated cholesterol efflux reduced cholesterol accumulation and suppressed tumor growth, while enhancing cytotoxic immune activity in the TME. Mechanistically, the YAP1-TEAD1 complex directly binds to the promoter regions of ABCG5 and ABCG8 and represses their transcription, thereby limiting cholesterol efflux and promoting intracellular cholesterol accumulation in HCC cells. DHA disrupted the YAP1-TEAD1 interaction, as further supported by SPR analysis, downregulated YAP1 and TEAD1, and restored ABCG5/G8-mediated cholesterol efflux. Notably, DHA-induced ABCG5/ABCG8 upregulation, cholesterol efflux, and antitumor effects were markedly attenuated by YAP1 inhibition, supporting a YAP1-dependent mechanism. In addition, DHA suppressed the growth and viability of organoids derived from patients with HCC.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;This study reveals that DHA disrupts the YAP1-TEAD1 interaction to relieve transcriptional repression of ABCG5/G8, thereby promoting cholesterol efflux, remodeling the tumor immune microenvironment toward enhanced cytotoxic T-cell activity, and enhancing anti-PD-1 immunotherapy in HCC. These findings provide a novel mechanism for DHA as an immunomo","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":"159 ","pages":"158584"},"PeriodicalIF":11.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148579774","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":"Theaflavin alleviates thoracic aortic dissection by disrupting the interaction between microtubule affinity-regulating kinase 4 and NLRP3 to inhibit inflammasome assembly.","authors":"Xing Chen, Shuying Xu, Tianhao Gu, Jintao Qian, Junhao Zhang, Yong Deng, Zhihua Wang, Jiahui Wang, Xinglong Tang, Chuiyu Kong, Qing Zhou","doi":"10.1016/j.phymed.2026.158502","DOIUrl":"10.1016/j.phymed.2026.158502","url":null,"abstract":"<p><strong>Background: </strong>Thoracic aortic dissection (TAD) is a severe vascular disorder characterized by structural damage, where macrophage-driven inflammation and NLRP3 inflammasome activation play pivotal roles. While the broad anti-inflammatory properties of Theaflavin (TF) are known, its precise structural targets within the TAD cascade remain incompletely understood. We hypothesized that TF protects against TAD by competitively disrupting the MARK4-NLRP3 interaction, thereby suppressing macrophage pyroptosis and inflammasome assembly.</p><p><strong>Purpose: </strong>To evaluate the therapeutic efficacy of TF in preventing the progression of TAD and to systematically elucidate its precise molecular and structural targets.</p><p><strong>Methods: </strong>A β-aminopropionitrile (BAPN)-induced murine TAD model was established to evaluate the efficacy of TF in mice. For Bone marrow-derived macrophages (BMDMs) and PMA-differentiated THP-1 macrophages, LPS and ATP stimulation was applied to activate the NLRP3 inflammasome. Transcriptomic sequencing, Western blot, immunofluorescence, co-immunoprecipitation (Co-IP), cellular thermal shift assay (CETSA), drug affinity responsive target stability (DARTS), and molecular docking were used to delineate TF's targets and mechanisms.</p><p><strong>Results: </strong>TF significantly reduced BAPN-induced mortality (from 40% to 15% at 20 mg/kg/d) and attenuated aortic dilation-decreasing the diameters of the ascending aorta, arch, and descending aorta by up to 17.0%, 29.2%, and 20.0%, respectively-by suppressing pro-inflammatory cytokines in mice. Mechanistically, TF directly bound to the NLRP3 NACHT domain (Gln359/Pro365 residues) to disrupt its interaction with MARK4, blocking NLRP3 trafficking to the microtubule organizing center (MTOC) and inflammasome assembly. TF also reduced GSDMD cleavage and pyroptosis, which was reversed by MARK4 overexpression.</p><p><strong>Conclusion: </strong>TF attenuates TAD pathogenesis by structurally disrupting the spatial assembly of NLRP3, thereby inhibiting the MARK4/NLRP3/GSDMD pyroptosis axis in macrophages.</p>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":"159 ","pages":"158502"},"PeriodicalIF":11.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148423477","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":"Inhibition of toll-like receptor 4 by allicin suppresses mitochondrial DNA-mediated inflammation and pyroptosis to alleviate myocardial ischemia-reperfusion injury.","authors":"Shichao Liang, Song Wu, Jiajie Yin, Tong Gao, Mengru Liu, Yijie Gao, Fangyuan Luo, Danni Wu, Songyuan Yu, Lin Zhao, Baofu Wang, Xianlun Li","doi":"10.1016/j.phymed.2026.158513","DOIUrl":"10.1016/j.phymed.2026.158513","url":null,"abstract":"<p><strong>Background: </strong>Mitochondrial DNA (mtDNA) leakage after myocardial ischemia/reperfusion (MI/R) injury activates inflammation and pyroptosis. Although toll-like receptor 4 (TLR4) is a known mediator of MI/R injury, its interplay with mtDNA remains unclear. This study investigates the cardioprotective mechanism of allicin, focusing on its disruption of the TLR4-mtDNA axis.</p><p><strong>Purpose: </strong>This study aimed to clarify the mechanisms of inflammatory response and pyroptosis in MI/R injury and the therapeutic targets of allicin.</p><p><strong>Methods: </strong>The cardioprotective mechanism of allicin was investigated in both in vivo and in vitro MI/R models. In Sprague-Dawley rats, different concentrations of allicin were administered pre-reperfusion. Myocardial injury, cytosolic mtDNA leakage, and activation of the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) and nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing 3 (NLRP3)-gasdermin D (GSDMD) pathways were assessed. Network pharmacology combined with molecular dynamics simulation identified TLR4 as a candidate signaling pathway for validation. In H9C2 cells subjected to OGD/R, the role of TLR4 in mtDNA-induced inflammatory response and pyroptosis, and the therapeutic mechanism of allicin, were studied using TLR4 agonist RS09 and inhibitor resatorvid. Myocardial injury markers, cytosolic mtDNA leakage, cGAS-STING and NLRP3-GSDMD pathway activity, and TLR4 expression were measured.</p><p><strong>Results: </strong>In vivo experiments demonstrated that allicin alleviated MI/R injury, suppressed cytosolic mtDNA leakage, and inhibited the cGAS-STING-mediated inflammatory response and the NLRP3-mediated pyroptosis pathways. Subsequent network pharmacology and molecular dynamics simulation identified TLR4 as a potential mediator of these effects. In vitro studies revealed that TLR4 activation promotes mtDNA-dependent inflammation and pyroptosis, which were effectively suppressed by allicin or TLR4 inhibition.</p><p><strong>Conclusion: </strong>TLR4 activation aggravates MI/R injury by promoting mitochondrial damage and cytosolic mtDNA leakage, which activates the pro-inflammatory (cGAS-STING) and pro-pyroptotic (NLRP3-GSDMD) pathways. Allicin protects against MI/R injury by inhibiting TLR4 activation and the subsequent mtDNA-induced pathways, thereby reducing inflammation and pyroptosis.</p>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":"159 ","pages":"158513"},"PeriodicalIF":11.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148397528","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}