Journal of Biochemical and Molecular Toxicology最新文献

{"title":"Knockdown of LINC00853 Inhibits the Progression and Immune Escape of Hepatocellular Carcinoma by Targeting the miR-16-5p/PD-L1 Axis.","authors":"Dong Wang, Fei Zhao, Lei Wang, Shaocong Yan","doi":"10.1002/jbt.70831","DOIUrl":"https://doi.org/10.1002/jbt.70831","url":null,"abstract":"<p><p>Long non-coding RNAs (lncRNAs) play crucial roles in hepatocellular carcinoma (HCC), offering valuable insights for therapeutic development. However, the clinical significance and functional mechanisms of LINC00853 in HCC remain poorly understood. This study aimed to evaluate the prognostic value of LINC00853 in HCC patients, and to investigate its underlying mechanisms in regulating HCC. A cohort of 123 HCC patients was enrolled in this study. LINC00853 expression in tumor tissues was quantified by quantitative reverse transcription-PCR (qRT-PCR). Prognostic significance of LINC00853 was assessed using Kaplan-Meier curves and Cox regression models. In vitro functional assays, including Cell Counting Kit-8 (CCK-8) and Transwell assays, were conducted to evaluate the effects of LINC00853 knockdown on cell proliferation, migration, and invasion. The regulatory axis involving LINC00853, miR-16-5p, and programmed death-ligand 1 (PD-L1) was validated by dual-luciferase reporter assays. The role of LINC00853 in immune escape was investigated by co-culturing CD8+ T cells with HCC cells and measuring cytotoxic activity along with cytokine (TNF-α, IFN-γ, IL-10, and TGF-β) levels. LINC00853 was significantly overexpressed in HCC tissues and was associated with unfavorable prognosis. Silencing LINC00853 suppressed the proliferation, migration, and invasion of HCC cells. Mechanistically, LINC00853 functioned as a molecular sponge for miR-16-5p, thereby upregulating PD-L1 expression. In the co-culture system, LINC00853 knockdown enhanced CD8+ T cell cytotoxicity and promoted the secretion of inflammatory cytokines (TNF-α and IFN-γ), while reducing immunosuppressive factors (IL-10 and TGF-β). These effects were reversed by the miR-16-5p inhibitor. LINC00853 may serve as a novel prognostic marker for HCC. Knockdown of LINC00853 suppresses the progression and immune escape by targeting the miR-16-5p/PD-L1 axis, suggesting its potential as a therapeutic target.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70831"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redox-Guided Metabolic Control in Cancer: Integration of the Reactive Oxygen Species-AMP-Activated Protein Kinase-Sirtuin Axis in Tumour Adaptation and Therapy.","authors":"Fathe Singh","doi":"10.1002/jbt.70851","DOIUrl":"10.1002/jbt.70851","url":null,"abstract":"<p><p>Cancer progression is tightly linked to metabolic reprogramming and persistent redox imbalance, which together sustain tumour growth while simultaneously creating exploitable vulnerabilities. Reactive oxygen species (ROS), once viewed solely as damaging metabolic by-products, are now recognized as dynamic signalling molecules that regulate energy homeostasis, mitochondrial function, and cell-fate decisions. Central to this regulation is the ROS-AMP-activated protein kinase (AMPK)-sirtuin axis, an evolutionarily conserved network that integrates redox signals with cellular energy sensing and NAD⁺ metabolism. AMPK responds to energetic and oxidative stress by suppressing anabolic pathways and promoting catabolic adaptation, whereas NAD⁺-dependent sirtuins-particularly SIRT1, SIRT3, and SIRT6-translate metabolic and redox cues into coordinated transcriptional, epigenetic, and mitochondrial responses. At moderate ROS levels, activation of this axis restores metabolic equilibrium, enhances antioxidant defences, and preserves genomic stability; in contrast, excessive or sustained oxidative stress overwhelms adaptive capacity, driving mitochondrial dysfunction and apoptosis in metabolically compromised tumour cells. This review provides a mechanistic and translational synthesis of how ROS regulate AMPK and sirtuin activity through both energy-dependent and redox-dependent mechanisms, thereby reshaping cancer metabolism and redox homeostasis. We examine the context-dependent roles of individual sirtuin isoforms across nuclear, cytosolic, and mitochondrial compartments and discuss emerging therapeutic strategies targeting this network, including pharmacological AMPK activators, NAD⁺ boosters, sirtuin modulators, and redox-active nutraceuticals. Finally, we highlight key translational challenges and future directions, emphasizing biomarker-guided precision, isoform-specific targeting, and controlled modulation of ROS signalling. Collectively, this framework positions the ROS-AMPK-Sirtuin axis as a foundation for redox-guided metabolic oncology.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70851"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147729149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"β-Sitosterol Restored Intestinal Barrier Integrity and Reduced Intestinal Hypermotility in Stress-Induced IBS: Comparison With Sertraline.","authors":"Sepideh Hajivand, Mohammadreza Sharifi, Ardeshir Talebi, Maedeh Ghasemi","doi":"10.1002/jbt.70789","DOIUrl":"https://doi.org/10.1002/jbt.70789","url":null,"abstract":"<p><p>Irritable bowel syndrome (IBS) is characterized by visceral hypersensitivity, intestinal hypermotility, and impaired barrier integrity. This study evaluated the effects of β-sitosterol and sertraline on colonic motility, tight junction proteins and chloride channel (ClC-2) expression, intestinal inflammation and endotoxemia in water avoidance stress (WAS)-induced rat model of IBS. Thirty-five male Wistar rats were divided into five groups (n = 7/group): control, WAS+β-sitosterol (25 mg/kg/day in olive oil), WAS + sertraline (30 mg/kg/day in saline), WAS + olive oil and WAS + saline groups. WAS (10 days) was used to induce IBS-like symptoms in rats. Fecal pellet output (FPO), fecal water content (FWC), and intestinal transit were assessed to determine motility and diarrhea. QRT-PCR quantified Claudin-1, Claudin-2, and ClC-2 mRNA expression. Endotoxemia and intestinal inflammation were assessed by measuring serum lipopolysaccharide (LPS) and colonic TNF-α level. WAS significantly increased FPO, FWC, and accelerated intestinal transit compared to control. Treatment with both β-sitosterol and sertraline reduced FPO and FWC compared to untreated IBS rats. β-sitosterol (but not sertraline) normalized intestinal transit. WAS significantly upregulated Claudin-2 and downregulated Claudin-1 compared to control. β-sitosterol restored Claudin-1/2 expression and upregulated ClC-2 above control levels. Sertraline increased Claudin-1 and ClC-2 but did not affect Claudin-2 compared to untreated IBS group. WAS caused significant colonic inflammation with a threefold TNF-α increase, confirming an IBS-like state. Sertraline and β-sitosterol significantly reduced TNF-α in colon tissue. β-sitosterol significantly reduced serum LPS and preserved colonic crypt architecture, wall thickness, and mucosa compared to untreated IBS group. Sertraline reduced TNF-α, LPS and improved wall thickness but did not affect crypt architecture or prevent erosion. β-Sitosterol alleviated hypermotility, restored barrier integrity, reduced inflammation and prevented endotoxemia. ClC-2 modulation and mucosal healing of β-sitosterol suggest its potential as a targeted IBS therapy.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70789"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147815529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective Effect of Saroglitazar Against Acute Lung Injury Induced by LPS in Rats.","authors":"Marina R Francis, Ahmed R El-Sheakh, Ghada M Suddek","doi":"10.1002/jbt.70879","DOIUrl":"https://doi.org/10.1002/jbt.70879","url":null,"abstract":"<p><p>Sepsis-induced acute lung injury (ALI) is a grave pathological syndrome correlated with high morbidity and fatality rates. This experiment investigated the prophylactic impact of saroglitazar (SAR) against acute lung injury induced through LPS injection. Prophylaxis with SAR (2 and 4 mg/kg) 2 weeks prior to LPS injection could alleviate LPS-induced ALI, as proved by the decline in lung tissue pathological injury. Total protein, LDH and TNF-α levels were also mitigated in BALF. Meanwhile, SAR attenuated LPS-related oxidative stress; it decreased MDA contents, while SOD activity and GSH contents were enhanced. Pulmonary contents of NF-κB, IFN-β, and SCG 3A2, were markedly reduced in SAR-pretreated rats. SAR exhibited a worthwhile influence against activation of canonical and non-canonical inflammasome and pyroptosis, induced by LPS, as shown through the decline in NLRP3, Caspase-1, GSDMD, Caspase-11, and IL-1β expression and activation. This research concluded that SAR could be a promising option in prophylaxis against LPS-induced ALI.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70879"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MARCH3 Inhibits Tumorigenesis and Enhances Paclitaxel Sensitivity in Nasopharyngeal Carcinoma by Ubiquitinating Hexokinase 2.","authors":"Xinggu Luo, Qingshan Jiang, Zhifeng Liu, Yuxiang Tan, Yilian Xu, Jing Peng","doi":"10.1002/jbt.70852","DOIUrl":"https://doi.org/10.1002/jbt.70852","url":null,"abstract":"<p><p>Glycolytic enzyme hexokinase 2 (HK2) plays a crucial role in the development of several human cancers, including nasopharyngeal carcinoma (NPC). This project is designed to explore the role and mechanism of HK2 in NPC progression. HK2 and membrane-associated RING-CH-type finger 3 (MARCH3) mRNA and protein levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR) and western blot. Cell viability, proliferation, migration, invasion, and apoptosis were measured using Cell Counting Kit-8 (CCK-8), Colony formation, wound healing, transwell, and flow cytometry. Glycolysis level was detected via specific kits. The stability of HK2 was assessed by Cycloheximide (CHX) assay. After Ubibrowser online database prediction, the interaction between MARCH3 and HK2 was validated using Co-immunoprecipitation (Co-IP) assay and GST pull-down assay. The effect of MARCH3 on PTX sensitivity of NPC was analyzed using in vivo studies. HK2 level was increased in NPC tissues and cell lines, and MARCH3 expression was decreased. Furthermore, HK2 knockdown repressed NPC cell proliferation, migration, invasion, glycolysis, and improved cell sensitivity to PTX. At the molecular level, MARCH3 could promote HK2 ubiquitination and decrease its stability. In addition, overexpressing MARCH3 increased the PTX sensitivity of NPC in vivo. MARCH3 could block NPC progression and strengthen the sensitivity of NPC cells to PTX, possibly by advancing the ubiquitination degradation of HK2, providing a promising therapeutic target for NPC treatment.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70852"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Protective Effects of Crocin and Pentoxifylline, Alone and in Combination, in Alleviating Acrylamide-Induced Hepatic Injury in NMRI Mice.","authors":"Yaser Mohammadi, Reyhaneh Taebi, Elham Bahreini, Mohammad Babaei, Asieh Hosseini","doi":"10.1002/jbt.70810","DOIUrl":"https://doi.org/10.1002/jbt.70810","url":null,"abstract":"<p><p>Acrylamide (ACR) is formed as a byproduct during high-temperature processing of carbohydrate-rich, low-protein foods and represents a widespread dietary contaminant. Given the extensive daily human exposure, its hepatotoxic potential is a growing concern. Therefore, this study aimed to evaluate the protective effects of crocin and pentoxifylline (PTX), administered individually or in combination, against ACR-induced hepatotoxicity in an animal model. Thirty male NMRI mice were randomly assigned to five groups (n = 6): normal, ACR, ACR + crocin, ACR + PTX, and ACR + crocin + PTX. Crocin (50 mg/kg) and PTX (50 mg/kg) were administered orally for 2 weeks. Hepatotoxicity was induced by a single intraperitoneal injection of ACR (10 μg/kg), and animals were euthanized 24 h later. Serum samples were collected for the assessment of liver function, oxidative stress, antioxidant defense, and inflammatory markers, while liver tissues were subjected to histopathological and molecular analyses. Crocin significantly reduced IL-6 (~19%) and increased CAT activity (~14%), whereas PTX decreased TNF-α levels and elevated GSH (~31.7%). In contrast, the combined crocin + PTX treatment exerted more pronounced protective effects, significantly reducing ALT and AST levels, lowering TNF-α (~31.25%) and IL-6 (~20.7%), and attenuating oxidative stress through reductions in MDA (~19.75%) and TOS (~17.5%), accompanied by a marked increase in TAC (~63.2%). This combination also enhanced CAT activity (~25%) and GSH levels (~44.4%), although SOD activity remained unchanged. At the gene expression level, none of the interventions fully restored Nrf2 or FOXO3a expression; however, PTX significantly upregulated FOXO3a expression, resulting in a ~26-fold increase compared to the ACR group, although levels remained markedly lower than those of the normal group. Histopathological evaluation revealed reduced hepatic damage in the treatment groups. Overall, these findings suggest that while crocin and PTX individually confer limited protection, their combined administration exerts a significant synergistic hepatoprotective effect against ACR-induced toxicity.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70810"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA SNHG14 Participates in the Development of Chronic Obstructive Pulmonary Disease by Targeting the miR-150-5p/BASP1 Axis.","authors":"Mayinuer Yibulayin, Xiaohong Yang","doi":"10.1002/jbt.70843","DOIUrl":"https://doi.org/10.1002/jbt.70843","url":null,"abstract":"<p><p>Chronic Obstructive Pulmonary Disease (COPD) is characterized by irreversible airflow limitation that usually progresses over time. SNHG14 is upregulated in the tissues with acute lung injury, but its role in COPD remains unknown. This study focuses on investigating the levels of SNHG14 in COPD and its potential predictive value for COPD, along with the molecular pathway through which SNHG14 influences COPD. This study included 110 patients diagnosed with COPD and 110 healthy controls. The levels of SNHG14 in serum and cells were detected by RT-qPCR. The predictive role of SNHG14 for COPD was analyzed using ROC curve. The HBE cells were treated with cigarette smoke extracts (CSE) to simulate the pathological environment of COPD. The impact of SNHG14 on HBE cell proliferation was examined via CCK-8 assay, the concentrations of proinflammatory factors and airway remodeling proteins in HBE cells were detected by ELISA kits. SNHG14 was upregulated in the serum of COPD patients, and its high expression may predict the occurrence of COPD in the early stage. Additionally, SNHG14 was associated with the severity of disease and level of inflammation in patients. In HBE cells exposed to CSE, SNHG14 expression increased. Knockdown of SNHG14 enhanced HBE cell proliferation and reduced inflammatory factors and airway remodeling proteins by modulating the miR-150-5p/BASP1 axis. Therefore, SNHG14 may serve as a diagnostic biomarker for COPD and influence the disease progression of COPD by regulating the miR-150-5p/BASP1 axis.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70843"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Octreotide Counteracts IFN-γ-Induced Endothelial Inflammation.","authors":"Saikat Fakir, Madan Sigdel, Md Matiur Rahman Sarker, Nektarios Barabutis","doi":"10.1002/jbt.70841","DOIUrl":"10.1002/jbt.70841","url":null,"abstract":"<p><p>Endothelial cells maintain vascular homeostasis through the regulation of permeability and coagulation. Interferon-gamma (IFN-γ), a proinflammatory cytokine released by activated T lymphocytes and natural killer cells, disrupts endothelial junctional integrity, leading to barrier dysfunction. Octreotide (OCT), a synthetic somatostatin analog (SSA), is used to suppress excessive growth hormone secretion and inhibits tumor growth. The present study investigates the potential anti-inflammatory and cytoprotective properties of OCT in IFN-γ-induced endothelial injury. Our observations suggest that OCT suppresses IFN-γ-induced activation of cofilin, MLC2, JAK2, STAT1, STAT3, and P38; as well as endothelial hyperpermeability and ROS generation. Hence, the study supports ongoing efforts aiming to substantiate the protective role of somatostatin analogs in endothelium-dependent disorders, including lung injury and sepsis.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70841"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13092887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147723008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TGFβ1 Inhibits Migration, Invasion, and Proliferation of HTR-8/Svneo Cells via tTG-Activated TLR4/NF-κB Signaling Pathway.","authors":"Mi Cheng, Xiaodan Di, Qiaozhu Chen, Taowei Dong, Fang Guo, Huiqian Zeng, Yanqin Zheng, Zequn Liu, Kun Shi","doi":"10.1002/jbt.70844","DOIUrl":"10.1002/jbt.70844","url":null,"abstract":"<p><p>TGFβ1 plays a key role in placental development, but its regulation of trophoblast function isn't fully known. Meanwhile, the TLR4/NF-κB pathway is linked to trophoblast dysfunction, yet the mediator linking TGFβ1 to this pathway is unclear. Thus, this study examines if tTG mediates TGFβ1's regulation of trophoblast functions via TLR4/NF-κB and its relevance in preeclampsia (PE). To address this, HTR-8/Svneo cells were treated with TGFβ1, cell migration, invasion, and proliferation were assessed via Transwell and CCK-8 assays. The expression of tTG, TLR4/NF-κB pathway components, and pro-inflammatory cytokines was evaluated by qPCR and Western blot. Gain- and loss-of-function approaches for tTG and TLR4 were employed, alongside transcriptome sequencing. The role of tTG's enzymatic activity was tested using the inhibitor Z-DON. Placental tissues from normal and preeclamptic pregnancies were analyzed for clinical validation. The results showed that TGFβ1 dose-dependently inhibited trophoblast migration, invasion, and proliferation while upregulating tTG expression. tTG overexpression activated the TLR4/NF-κB pathway and altered the transcriptome. TLR4 inhibition blocked tTG-mediated NF-κB activation. Furthermore, tTG knockdown and inhibiting tTG's enzymatic activity reversed the suppressive effects of TGFβ1 on cell functions and downstream TLR4/NF-κB signaling. Clinically, the protein levels of tTG and activated TLR4/NF-κB pathway components were significantly elevated in preeclamptic placentas. In conclusion, this study first reveals a TGFβ1/tTG/TLR4/NF-κB axis in trophoblasts, showing TGFβ1 inhibits trophoblast function via upregulation of tTG, which functionally leads to activation of the TLR4/NF-κB pathway in an enzyme activity-dependent manner, providing new insights into PE pathogenesis and potential therapeutic targets.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70844"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147729173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cinnamaldehyde Attenuates Collagen-Induced Arthritis in Rats Through Immunomodulation and Alteration of Intestinal Flora Homeostasis and Repair of Intestinal Barrier Damage.","authors":"Shuai Wang, Wanqing Dai, Yue Liu, Xingyu Zou, Mengjun Pan, Xiaoqin Chu","doi":"10.1002/jbt.70891","DOIUrl":"https://doi.org/10.1002/jbt.70891","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a complex autoimmune disease, the present study aimed to investigate the effects of cinnamaldehyde (CA) on collagen-induced arthritis (CIA) in rats, with particular attention to changes in intestinal barrier-related features, gut microbiota composition, and fecal short-chain fatty acids (SCFAs). In CIA rats, CA treatment alleviated arthritis-related signs, reduced inflammatory responses, and attenuated joint pathological damage. CA administration was also associated with restoration of intestinal barrier-related features, including restoration of colonic histopathology and mucus layer integrity, as well as increased expression of tight junction proteins. Moreover, CA treatment was associated with altered gut microbiota composition. At the genus level, CA intervention was associated with increased abundance of Akkermansia, Ligilactobacillus, and Ruminococcaceae, which were negatively correlated with arthritis severity. CA treatment was associated with increased fecal SCFA levels in CIA rats. Collectively, these findings indicate that CA administration is associated with normalization of the gut microbiota, enhancement of intestinal barrier function, and amelioration of arthritis symptoms in CIA rats, suggesting that the interplay among gut dysbiosis, intestinal barrier damage, and arthritis may represent a contributing factor in the pathogenesis of RA.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70891"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}