Journal of Molecular Histology最新文献

{"title":"Comparison of the efficacy of TXNDC5 monoclonal antibody versus conventional drugs in the treatment of intestinal fibrosis associated with inflammatory bowel disease","authors":"Jiawei Liu,&nbsp;Lin Zhang,&nbsp;Xianghui Li,&nbsp;Mi Yang","doi":"10.1007/s10735-026-11005-9","DOIUrl":"10.1007/s10735-026-11005-9","url":null,"abstract":"<div><p>To compare the therapeutic efficacy of a thioredoxin domain-containing protein 5 (TXNDC5) monoclonal antibody (mAb) against prednisolone and sulfasalazine in DSS-induced IBD-related intestinal fibrosis mouse models. A total of 48 C57BL/6 mice were randomly divided into four model groups (Group A–D, 12 animals per group), while seven extra mice were assigned to the blank control group. Intestinal fibrosis was induced in mice of Groups A to D via recurrent administration of 2% DSS solution. On day 26 post-modeling, five mice from each model group were sacrificed to validate model success, and the leftover animals were treated with corresponding drugs or saline for 14 successive days. Multiple detection indexes were assessed in this study, consisting of body weight, DAI score, colonic morphological features, serum levels of transforming growth factor-β (TGF-β) and tumor necrosis factor-α (TNF-α), collagen deposition level as well as colonic TXNDC5 expression. One-way ANOVA coupled with Tukey’s post hoc test was applied for all statistical analyses. The TXNDC5 mAb group presented better weight restoration and earlier DAI remission. It obtained longer colon length, lower colon weight, decreased serum inflammatory cytokines and milder collagen accumulation relative to the two conventional drug groups (all <i>P</i> &lt; 0.05). Meanwhile, TXNDC5 mRNA and protein expression were significantly downregulated in the mAb group compared with prednisolone and sulfasalazine groups. No statistical difference was found between the two traditional medication groups. At the experimental doses adopted in the present study, TXNDC5 mAb showed more pronounced anti-inflammatory and anti-fibrotic effects than prednisolone in DSS-induced mice. However, due to the potentially sub-therapeutic sulfasalazine dose, its comparative superiority over sulfasalazine cannot be established from the current data. These findings should be considered preliminary and hypothesis-generating, requiring further validation in optimized experimental settings.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149176733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Autophagy hub genes mediate photodynamic therapy tolerance in nasopharyngeal carcinoma through cytoprotective autophagy and survival signalling","authors":"Ya Peng,&nbsp;Xiaowen Deng,&nbsp;Hanbing Yao,&nbsp;Jiaodi Cai,&nbsp;Jian Kang","doi":"10.1007/s10735-026-10998-7","DOIUrl":"10.1007/s10735-026-10998-7","url":null,"abstract":"","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-026-10998-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149176458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Wound healing potential of Sarcophaga aegyptiaca larval excretion/secretion: in vivo assessment of inflammatory biomarkers and in silico molecular docking study","authors":"Nancy Taha Mohammed,&nbsp;Heba El-Sayed,&nbsp;Amina Osama Ghannam,&nbsp;Hager Waled Hussien,&nbsp;Olfat A. Hammam,&nbsp;Amina M. Ibrahim,&nbsp;Marwa A. Hamada,&nbsp;Mostafa Y. Morad","doi":"10.1007/s10735-026-10996-9","DOIUrl":"10.1007/s10735-026-10996-9","url":null,"abstract":"<div><p>The quality of life is significantly impacted by cutaneous ulcers, which frequently develop into chronic conditions. As the need for managing chronic wounds grows, interest in larval therapy (LT), an intervention that uses live fly larvae and/or their secretion to eliminate necrotic tissue and encourage healing, has increased. The present study aimed to investigate the wound healing potential of <i>Sarcophaga aegyptiaca</i> larval excretion/secretion (ES) with particular emphasis on its antioxidant activity, tissue regenerative capacity, and bioactive compound composition. Using a mice full-thickness excisional wound model, we evaluated the effects of the topical application of the larval extract on wound closure dynamics, oxidative stress biomarkers, and histological outcomes over a 15-day treatment period. Gas chromatography–mass spectrometry (GC–MS) analysis of the larval ES identified a diverse array of bioactive molecules, dominated by myristic acid vinyl ester, unsaturated fatty acid esters, terpenoid alcohols, and spirocyclic diketones—compounds recognized for their antimicrobial, anti-inflammatory, and tissue-reparative properties. Macroscopic assessments revealed markedly enhanced wound contraction in the treated group compared to negative controls. The larva-treated group demonstrated substantial healing early on and achieved an impressive 98.14% wound closure by day 15. Biochemical analysis indicated a pronounced early increase in Total Antioxidant Capacity (TAC) following treatment, implicating oxidative stress modulation as a key mechanism. Although changes in other oxidative stress biomarkers such as nitric oxide (NO) were less prominent at later stages, the early antioxidant response appeared to correlate with enhanced healing outcomes, while malondialdehyde (MDA) of the larvae ES-treated group showed a significant decrease in its level after 7 days of treatment. In addition, the proinflammatory cytokines TNF-α and IL-1β were markedly decreased in the larvae ES-treated group as compared to negative controls. Histological evaluations supported these findings, showing reduced inflammatory cell infiltration, increased collagen deposition, and advanced re-epithelialization in the larvae-treated group. The molecular docking interaction demonstrated high efficiency for acid vinyl ester against the TNF-α and IL-1β cytokines revealing a potential efficacy of this compound on the proinflammatory cytokines. These results demonstrated that <i>S. aegyptiaca</i> larval ES exerts a multifaceted therapeutic effect on wound healing through bioactive compound-mediated tissue regeneration and early oxidative stress modulation.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149176732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liraglutide ameliorates obese type 2 diabetes by regulating macrophage cholesterol metabolism and H3K27ac modification to promote M2 polarization and adipocyte thermogenic activation","authors":"Ping Wang,&nbsp;Jie Zhang,&nbsp;Weifeng Zhou,&nbsp;Nan Zhang,&nbsp;Yiqing Chen","doi":"10.1007/s10735-026-10993-y","DOIUrl":"10.1007/s10735-026-10993-y","url":null,"abstract":"&lt;div&gt;&lt;p&gt;Obesity-related type 2 diabetes mellitus (O&amp;T2DM) has become a major global public health issue. Chronic low-grade inflammation in adipose tissue is one of its core pathological features, among which excessive infiltration of M1-type macrophages and impaired function of M2-type macrophages are key drivers of inflammation. Liraglutide, a glucagon-like peptide-1 receptor agonist, exhibits significant glucose-lowering, weight-reducing, and anti-inflammatory effects. However, the molecular mechanisms by which liraglutide regulates cholesterol metabolism and epigenetic modifications in adipose tissue macrophages remain to be fully elucidated. A high-fat diet combined with streptozotocin was used to establish an O&amp;T2DM model in male C57BL/6 mice. After 8 weeks of intervention, metabolic phenotypes, adipose tissue macrophage polarization, and cholesterol metabolism-related indicators were assessed. Raw264.7 macrophages were cultured in vitro and stimulated with IFN-γ + LPS to induce M1 polarization. Following liraglutide pretreatment, cell polarization phenotypes, the expression of genes involved in cholesterol metabolic pathways, and histone modification levels were examined. Using shRNA gene silencing, p300 inhibitor intervention, and Acetyl-CoA supplementation experiments in combination with ChIP-qPCR, the central role of the cholesterol metabolism-epigenetic axis in macrophage polarization was elucidated. Finally, a Transwell co-culture system was employed to verify the regulatory effects of liraglutide-reprogrammed macrophages on adipocyte lipid accumulation and energy metabolism. Liraglutide significantly reduced body weight, fasting blood glucose, and HOMA-IR in O&amp;T2DM mice, decreased visceral fat accumulation, and promoted adipose tissue browning. It also increased the proportion of M2 macrophages within adipose tissue and significantly activated the key cholesterol efflux pathway LXRα/ABCA1. In vitro experiments confirmed that liraglutide pretreatment suppressed IFN-γ + LPS-induced M1 polarization and promoted the expression of M2-type markers, upregulated the expression of ABCA1, ABCG1, PPARγ, and LXRα, and increased levels of histone H3K27ac. Mechanistic studies revealed that silencing ABCA1 or LXRα reversed the liraglutide-induced increase in H3K27ac and M2 polarization. Acetyl-CoA supplementation partially restored the macrophage polarization phenotype following ABCA1 silencing. ChIP-qPCR results showed that liraglutide significantly enhanced the enrichment of H3K27ac in the promoter regions of M2 polarization genes and cholesterol metabolism genes. Co-culture experiments demonstrated that liraglutide-reprogrammed macrophages significantly promoted adipocyte thermogenic gene expression, increased mitochondrial membrane potential-dependent staining intensity, and enhanced ATPase activity via paracrine signaling, an effect that was blocked by silencing ABCA1 or LXRα. This study demonstrates that liraglutide activates the A","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-026-10993-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149176542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA SNHG8 contributes to post-myocardial infarction cardiac fibrosis and is functionally associated with miR-192-3p","authors":"Chao Yang,&nbsp;Mengyan Li,&nbsp;Tao Su,&nbsp;Di Jia,&nbsp;Han Gao,&nbsp;Hongyan Guo,&nbsp;Yan Shi,&nbsp;Shuyan Li,&nbsp;Zhenglin Zhao,&nbsp;Chunjing Zhang","doi":"10.1007/s10735-026-10999-6","DOIUrl":"10.1007/s10735-026-10999-6","url":null,"abstract":"<div><p>Cardiac fibrosis is a major contributor to adverse ventricular remodeling after myocardial infarction (MI), but the non-coding RNA networks involved in fibroblast responses remain incompletely understood. We investigated the role of the long non-coding RNA SNHG8 in post-infarction cardiac fibrosis and its relationship with miR-192-3p using a murine MI model and angiotensin II (Ang II)-stimulated cardiac fibroblasts. SNHG8 expression was significantly increased in infarcted myocardium and in Ang II-treated fibroblasts. SNHG8 silencing reduced fibroblast proliferation and the expression of α-smooth muscle actin and collagen I, whereas SNHG8 overexpression produced the opposite effects in cultured fibroblasts. Dual-luciferase and rescue experiments supported a functional relationship between SNHG8 and miR-192-3p in vitro; however, these experiments do not establish an endogenous ceRNA mechanism or a validated downstream effector. In vivo, SNHG8 knockdown reduced post-MI scar burden and collagen I-positive area and partially preserved left ventricular systolic function. The role of miR-192-3p in mediating these in vivo effects was not tested. Together, the findings support a profibrotic role for SNHG8 in experimental post-MI remodeling and identify the SNHG8–miR-192-3p relationship as a candidate mechanism requiring further biochemical and in vivo validation.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149176612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Surfactant protein A (SP-A) alleviates acute kidney injury by reducing macrophage recruitment and M1 polarization","authors":"Jiayun Zhang,&nbsp;Jinjing Guo,&nbsp;Jie Fu,&nbsp;Dahui Wang","doi":"10.1007/s10735-026-10992-z","DOIUrl":"10.1007/s10735-026-10992-z","url":null,"abstract":"<div><p>Acute kidney injury (AKI) is a severe clinical condition characterized by rapid renal function decline and intense intrarenal inflammation. Surfactant Protein A (SP-A), known for its pulmonary immunomodulatory roles, is investigated here for its therapeutic potential in AKI recovery. Using a male C57BL/6J mouse model of bilateral renal pedicle clamping, we demonstrate that an SP-A agonist significantly preserves renal function, reducing serum creatinine and urea nitrogen levels, and attenuates histopathological tissue damage. Mechanistically, SP-A activation suppresses the infiltration of CD11b⁺F4/80⁺ macrophage, while shifting polarization by decreasing the proportion of F4/80⁺iNOS⁺ M1 cells and increasing that of F4/80⁺CD206⁺ M2 cells both in vivo and in vitro. In lipopolysaccharide (LPS)-stimulated RAW 264.7 cells, SP-A knockdown increases the secretion of TNF-α, IL-6, and IL-1β, and enhances cell migration ability, whereas SP-A treatment reverses these effects. These actions are mediated via inhibiting the NF-κB signaling pathway. Clodronate liposome-mediated macrophage depletion demonstrates that SP-A exerts its therapeutic effects, to some extent, through the mediation of macrophage. Co-culture of SP-A-pretreated RAW 264.7 cells with HK-2 cells revealed that SP-A-treated RAW 264.7 cells inhibit Kim-1 expression, and increase IGF-1 expression. Collectively, these findings reveal that SP-A reduces macrophage recruitment, suppresses M1 macrophage polarization, alleviates inflammation, and ameliorates AKI via the NF-κB pathway, offering a promising therapeutic target for AKI.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 5","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149132683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protein acylation and bone metabolism: bidirectional crosstalk linking metabolic reprogramming to skeletal homeostasis","authors":"Bingqi Wei,&nbsp;Yijing Li,&nbsp;Yuntan Li,&nbsp;Xinyue Zhang,&nbsp;Shangyuan Ge,&nbsp;Hejia Wan,&nbsp;Xiaobao Wang,&nbsp;Jingyuan Tian,&nbsp;Shangzeng Wang","doi":"10.1007/s10735-026-11002-y","DOIUrl":"10.1007/s10735-026-11002-y","url":null,"abstract":"<div><p>Protein acylation is an important class of post-translational modifications that uses acyl-coenzyme A (acyl-CoA) metabolites as donor substrates. Regulated by writers, erasers, and readers, these modifications dynamically control protein activity, stability, localization, and signaling, thereby linking cellular metabolism to functional adaptation. Bone homeostasis depends on the balance between osteoblast-mediated bone formation and osteoclast-driven bone resorption. Emerging evidence indicates that protein acylation is not only a regulator of skeletal remodeling, but also a metabolic sensor shaped by bone-cell reprogramming. In this review, we summarize the metabolic origins, regulatory enzymes, and skeletal functions of major acylation modifications, including acetylation, succinylation, lactylation, and palmitoylation. These modifications influence osteoblast differentiation, osteoclastogenesis, mitochondrial homeostasis, and microenvironmental adaptation through key targets such as Runx2, Osterix, p53, and superoxide dismutase 2 (SOD2). Conversely, metabolic transitions in bone cells, including enhanced glycolysis, mitochondrial activation, fatty acid oxidation, and tricarboxylic acid (TCA) cycle remodeling, reshape intracellular acyl-CoA availability and thereby alter cellular acylation patterns. This bidirectional crosstalk forms a dynamic metabolism–acylation–function axis whose dysregulation may contribute to osteoporosis, osteoarthritis, and other skeletal disorders. Understanding this regulatory network may provide candidate biomarkers and therapeutic targets for precision management of metabolic bone diseases.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 5","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149102315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Viburnum opulus protects against acetaminophen-induced splenic injury through coordinated antioxidant and anti-inflammatory responses","authors":"Buse Birinci,&nbsp;Nevruz Alis,&nbsp;Onur Onguncan,&nbsp;Nilay Seyidoglu,&nbsp;Sabire Guler","doi":"10.1007/s10735-026-10995-w","DOIUrl":"10.1007/s10735-026-10995-w","url":null,"abstract":"<div><p>Acetaminophen (APAP) overdose induces systemic oxidative and inflammatory responses, yet its effects on splenic homeostasis remain poorly characterized. We investigated whether prophylactic <i>Viburnum opulus L</i>. protects against APAP-induced splenic injury and the molecular pathways potentially underlying this protection. Forty female Wistar rats were allocated to control, APAP, N-acetylcysteine (NAC), <i>V. opulus</i> 100 (VO-100), and 300 mg/kg (VO-300) groups. NAC or <i>V. opulus</i> was administered orally for seven days, followed by a single oral APAP dose of 3 g/kg. Splenic histomorphology and immunohistochemical expression of cleaved Caspase-3, Ki-67, NF-κB, iNOS, SOD1, NRF2, and GPX4 were evaluated; network pharmacology and independent splenic transcriptomic analyses contextualized the experimental findings. APAP disrupted white- and red-pulp organization, induced lymphoid depletion, follicular disorganization, congestion, and sinusoidal dilatation, and significantly altered all seven markers, increasing cleaved Caspase-3, NF-κB, and iNOS immunoreactivity while reducing Ki-67, SOD1, and NRF2. GPX4 also decreased, but the control-APAP comparison lost significance after multiple-testing correction. VO-300 markedly attenuated the histomorphological alterations, reduced inflammatory and apoptosis-associated marker expression, and increased proliferative and antioxidant markers toward control levels. Network pharmacology identified 44 shared targets between major <i>V. opulus</i> constituents and APAP-toxicity-associated genes, with AKT1, NFKB1, PTGS2, and STAT3 as key hub proteins linked to oxidative-stress, apoptotic, and NF-κB-related pathways; 28 of these targets were confirmed in independent spleen transcriptomic data. Prophylactic <i>V. opulus</i>, particularly at 300 mg/kg, therefore, limits APAP-induced splenic injury by preserving tissue architecture, proliferative activity, and antioxidant defenses while attenuating inflammatory and apoptosis-associated responses.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 5","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149102487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apigenin attenuates MASLD progression by suppressing lipogenesis and macrophage M1-like inflammatory activation: involvement of SMAD4-associated signaling","authors":"Lijun Cao,&nbsp;Yongna Zhao,&nbsp;Ping Li","doi":"10.1007/s10735-026-11000-0","DOIUrl":"10.1007/s10735-026-11000-0","url":null,"abstract":"<div><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by dysregulated hepatic lipid metabolism and persistent inflammatory remodeling. Apigenin has lipid-regulatory and anti-inflammatory activities, but the molecular basis linking these effects remains incompletely understood. This study investigated whether SMAD4-associated signaling contributes to the coordinated regulation of hepatocyte lipogenesis and macrophage inflammatory activation by apigenin. C57BL/6J mice were fed a high-fat diet (HFD) to establish MASLD and treated with apigenin. Palmitic acid (PA)-treated HepG2 cells and lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages were used as complementary in vitro models. Hepatic lipid accumulation, inflammatory responses, macrophage phenotype, and SMAD4-associated signaling were evaluated using biochemical assays, histological staining, ELISA, RT-qPCR, Western blotting, immunohistochemistry, and immunofluorescence. Molecular docking was used to predict the potential interaction between apigenin and SMAD4, a cellular thermal shift assay (CETSA) was performed in HepG2 cells to assess cellular target engagement of SMAD4 by apigenin, and SMAD4/Smad4 overexpression was used to evaluate functional involvement. Apigenin alleviated HFD-induced liver injury, dyslipidemia, and hepatic lipid deposition and suppressed the SREBP-1c/FAS/ACC lipogenic program in mouse liver and PA-treated HepG2 cells. Apigenin also reduced hepatic CD68-positive macrophage accumulation, decreased CD86 and iNOS expression and pro-inflammatory cytokine levels, and attenuated M1-like inflammatory activation in vivo and in LPS-stimulated RAW264.7 macrophages. Molecular docking predicted a favorable interaction between apigenin and SMAD4, while CETSA demonstrated increased thermal stability of SMAD4 following apigenin exposure in HepG2 cells, supporting cellular target engagement in this cellular context. Apigenin further attenuated SMAD4-associated signaling, whereas SMAD4/Smad4 overexpression partially counteracted its anti-lipogenic and anti-inflammatory effects in HepG2 cells and RAW264.7 macrophages, respectively. These findings indicate that apigenin alleviates HFD-induced MASLD by coordinately suppressing hepatocellular lipogenesis and macrophage-associated inflammatory activation and suggest that SMAD4-associated signaling contributes to these metabolic and inflammatory effects.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 5","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149102653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gastroprotective effects of ethanolic leaf extracts of Matricaria chamomilla L. and Albizia lebbeck L. against indomethacin-induced gastric ulcer in Wistar rats: modulation of oxidative stress and inflammatory cytokines","authors":"Mohd Vaseem,&nbsp;Vidhu Aeri,&nbsp;Manju Sharma","doi":"10.1007/s10735-026-10997-8","DOIUrl":"10.1007/s10735-026-10997-8","url":null,"abstract":"<div><p>Indomethacin-induced gastric ulceration involves oxidative stress, inflammation, and impairment of gastric mucosal defense. This study evaluated the gastroprotective effects of ethanolic leaf extracts of <i>Matricaria chamomilla</i> L. (MC) and <i>Albizia lebbeck</i> L. (AL), individually and in combination, in an indomethacin-induced gastric ulcer model in Wistar rats. Animals were randomly divided into 11 experimental groups (<i>n</i> = 6 per group) and treated orally for 10 days with MC or AL (250 or 500 mg/kg), their combinations (total doses of 250 or 500 mg/kg), or ranitidine (50 mg/kg). Gastric injury was assessed by ulcer index, gastric mucus, oxidative stress markers, inflammatory cytokines, PGE₂, and histopathology. HPTLC fingerprinting supported the qualitative presence of rutin in MC and quercetin in AL. Indomethacin increased the ulcer index to 2.24 ± 0.24 and reduced gastric mucus to 1.45 ± 0.23 µg/g. The 500 mg/kg MC + AL combination reduced the ulcer index to 1.02 ± 0.13, increased gastric mucus to 2.66 ± 0.13 µg/g, decreased TBARS to 2.58 ± 0.14 nmol/mg protein, and increased GSH to 353.09 ± 24 µg/mg protein. TNF-α, IL-1β, and IL-6 decreased from 54 ± 3.1, 31 ± 1.6, and 23 ± 1.8 to 17 ± 0.9, 15 ± 0.7, and 7 ± 0.8 pg/mL, respectively, while PGE₂ increased from 11 ± 1.0 to 25 ± 1.4 pg/mL (<i>p</i> &lt; 0.01). Histopathology supported preservation of gastric mucosal architecture. Overall, MC and AL extracts exhibited gastroprotective effects associated with attenuation of oxidative and inflammatory responses and preservation of mucosal defense.</p><h3>Graphical Abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 5","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149101759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}