Journal of Molecular Histology最新文献

{"title":"Evaluation of miR-155-5p expression and ovarian histopathological changes in a cyclophosphamide-induced mouse model of premature ovarian insufficiency","authors":"Zahra Saadatian,&nbsp;Shadan Navid,&nbsp;Ali Talebi,&nbsp;Nasim Khajavian,&nbsp;Hanieh Babapour Chalaki","doi":"10.1007/s10735-026-11025-5","DOIUrl":"10.1007/s10735-026-11025-5","url":null,"abstract":"<div><h3>Background</h3><p>Premature ovarian insufficiency (POI) is a reproductive disorder characterized by amenorrhea, reduced estrogen levels, and elevated gonadotropins. Increasing evidence highlights the involvement of microRNAs, particularly miR-155-5p, in inflammation and apoptosis. This study aimed to evaluate the expression level of miR-155-5p and key folliculogenesis genes. Anti‐Müllerian hormone(AMH) and growth differentiation factor 9 (GDF9) in the ovarian tissue of a cyclophosphamide-induced POI mouse model compared with healthy controls, alongside histopathological assessment and follicle quantification.</p><h3>Methods</h3><p>Sixteen female NMRI mice were randomly assigned to two groups (n = 8 each). The experimental group received intraperitoneal cyclophosphamide (120 mg/kg) to induce POI, while the control group received normal saline. Ovarian tissues were harvested for molecular and histological analyses. Total RNA was extracted and subjected to cDNA synthesis, and miR-155-5p, AMH, and GDF9 expression were quantified by QRT-PCR. For morphological evaluation, serial ovarian sections were stained with hematoxylin–eosin (H&amp;E), toluidine blue, and Periodic Acid–Schiff (PAS) special stains.</p><h3>Results</h3><p>miR-155-5p expression was significantly upregulated in the POI group compared with controls (<i>P</i> &lt; 0.001). AMH expression was markedly downregulated (<i>P</i> &lt; 0.001) and GDF9 expression was significantly upregulated (<i>P</i> &lt; 0.05). Histopathology revealed reduced healthy follicles, increased atresia, stromal disruption, and oocyte degeneration in the POI group. Serum estradiol decreased, while FSH levels increased.</p><h3>Conclusion</h3><p>Upregulation of miR-155-5p was associated with ovarian histopathological alterations and changes in folliculogenesis-related gene expression in the cyclophosphamide-induced POI model. These findings identify miR-155-5p as a potential candidate biomarker of ovarian injury in this experimental setting. However, the present findings do not establish a causal or mechanistic role for miR-155-5p. Further functional studies, including gain- and loss-of-function experiments and target validation, as well as clinical studies, are required to determine its biological and clinical significance.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149316961","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":"FBXO17 promotes osteosarcoma progression by regulating glycolysis and macrophage polarization","authors":"Teng Zeng,&nbsp;Hao Chen","doi":"10.1007/s10735-026-10983-0","DOIUrl":"10.1007/s10735-026-10983-0","url":null,"abstract":"&lt;div&gt;&lt;p&gt;Osteosarcoma (OS) is the most common primary malignant bone tumor, characterized by high aggressiveness and poor prognosis. Glycolytic reprogramming and immune microenvironment imbalance contribute to OS progression, but the role of E3 ubiquitin ligases in coordinating glycolysis and macrophage polarization remains unclear. This study aimed to identify key E3 ubiquitin ligases regulating glycolysis and immune microenvironment in OS. Differentially expressed genes (DEGs) were identified from the GSE309091 lncRNA-sequencing dataset using DESeq2. Glycolysis-related genes from GeneCards and E3 ubiquitin ligases from UbiBrowser were integrated with DEGs, and Random Forest machine learning was applied to select core genes. Immune cell infiltration was assessed using CIBERSORT. Key gene expression was analyzed across the GSE309091 and GSE36001 datasets, with protein expression validated via Western blot. OS cell proliferation, cell cycle, apoptosis, invasion, and glycolysis were evaluated using colony formation, EdU, flow cytometry, Transwell assays, and glucose/lactate measurements. THP1-derived macrophages co-cultured with OS cell-conditioned medium were used to assess M1/M2 polarization. The expression of inflammatory cytokines was detected using ELISA. Potential FBXO17 substrates were predicted using UbiBrowser 2.0, and its regulatory relationship with PGC-1α was examined using Co-IP, ubiquitination, CHX-chase. Xenograft mouse models determined in vivo effects of FBXO17. FBXO17, SIAH2, BRCA1, and TRIM32 were identified as core genes associated with glycolysis and ubiquitination. Immune infiltration analysis showed their expression correlated with immune cell composition in OS. FBXO17 was highly expressed in GSE309091 and GSE36001 datasets, as well as in OS cell lines. FBXO17 knockdown inhibited OS cell proliferation, invasion, and glycolytic activity, induced G0/G1 arrest, promoted apoptosis, and enhanced M1 polarization of THP1 macrophages. FBXO17 interacted with PGC-1α and promoted its polyubiquitination and degradation. FBXO17 knockdown slowed PGC-1α degradation, whereas FBXO17 overexpression in FBXO17-knockdown cells reduced PGC-1α protein accumulation and partially restored lactate production. In vivo, FBXO17 silencing significantly suppressed tumor growth. FBXO17 promotes OS progression and glycolytic reprogramming, at least in part, by facilitating the ubiquitination and degradation of PGC-1α and is also involved in regulating macrophage polarization. Therefore, FBXO17 may represent a potential therapeutic target for OS.&lt;/p&gt;&lt;h3&gt;Graphical abstract&lt;/h3&gt;&lt;div&gt;&lt;figure&gt;&lt;div&gt;&lt;div&gt;&lt;picture&gt;&lt;source&gt;&lt;img&gt;&lt;/source&gt;&lt;/picture&gt;&lt;/div&gt;&lt;div&gt;&lt;p&gt;FBXO17 promotes OS progression by regulating glycolytic reprogramming and M2 macrophage polarization: This study systematically identified FBXO17 as a core candidate gene in OS through transcriptomic analysis integrated with machine learning, and demonstrated that FBXO17 promoted glycolysis and drove macrophage ","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149316962","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":"Circ_0018814 promotes the osteogenic differentiation of mesenchymal stem cells in ankylosing spondylitis by regulating the miR-944/KLF4 axis","authors":"Xi Chen,&nbsp;Jing Xie,&nbsp;Yanju Li,&nbsp;Xu Chen,&nbsp;Yuanyuan Liu,&nbsp;Donggeng Guo","doi":"10.1007/s10735-026-11019-3","DOIUrl":"10.1007/s10735-026-11019-3","url":null,"abstract":"<div><p>Ankylosing spondylitis (AS) is a chronic inflammatory disease primarily affecting the spine and sacroiliac joints. This study investigated the impact of circ_0018814 on the osteogenic differentiation of mesenchymal stem cells (MSCs) in AS through the regulation of the miR-944/KLF4 axis and to evaluate its potential role in the progression of AS. GSE203155 was used as an exploratory screening dataset to identify candidate circRNAs associated with osteogenic differentiation in AS-MSCs. Circ_0018814 expression was further evaluated in bone marrow samples and primary MSCs. The effects of circ_0018814 on osteogenic differentiation markers (ALP, RUNX2, COL1A1) in MSCs from AS patients were assessed using western blot, ALP assay, and alizarin red S staining. The targeting relationship between circ_0018814, KLF4, and miR-944 was confirmed through luciferase reporter and RNA immunoprecipitation assays. Fluorescence in situ hybridization was used for cellular localization. Further experiments in a murine AS model evaluated the impact of circ_0018814 on AS lesions and MSC differentiation. The results showed that overexpression of circ_0018814 significantly enhanced the expression of osteogenic markers ALP, RUNX2, and COL1A1, and promoted the osteogenic differentiation of MSCs. Additionally, circ_0018814 regulated KLF4 expression by targeting miR-944. Inhibition of miR-944 upregulated KLF4 expression and promoted osteogenic differentiation. In the AS mouse model, downregulation of circ_0018814 significantly alleviated spinal lesions, restored normal expression levels of miR-944 and KLF4, and reduced disease-related osteogenic changes. This study demonstrates that circ_0018814 plays an important role in the pathological progression of AS by regulating the miR-944/KLF4 axis. circ_0018814 may serve as a novel potential therapeutic target for AS, providing new insights for future treatment strategies. However, the in vivo findings should be interpreted cautiously because tail vein delivery of lentiviral constructs is not MSC-specific.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13724634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149316960","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":"Correction: Extracellular matrix assembly during chondrogenic differentiation of amniotic fluid- and adipose-derived mesenchymal stromal cells under TGF-β3 induction","authors":"Carolina Coli Zuliani,&nbsp;Ingrid Iara Damas,&nbsp;Kleber Cursino de Andrade,&nbsp;Paulo Kharmandayan,&nbsp;Ângela Maria Moraes,&nbsp;Ali Mobasheri,&nbsp;Ibsen Bellini Coimbra","doi":"10.1007/s10735-026-11022-8","DOIUrl":"10.1007/s10735-026-11022-8","url":null,"abstract":"","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13722795/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149293800","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":"Germacrone inhibits podocyte pyroptosis in diabetic kidney disease by modulating ABCA1 expression","authors":"Binqi Wang,&nbsp;Bo Lin,&nbsp;Jiang Chen,&nbsp;Li Zhao,&nbsp;Yali Ye,&nbsp;Danna Zheng","doi":"10.1007/s10735-026-11020-w","DOIUrl":"10.1007/s10735-026-11020-w","url":null,"abstract":"<div><p>Diabetic kidney disease (DKD) is a serious microvascular complication of diabetes with limited treatment strategies. Germacrone (Ger) has renoprotective properties, but its molecular targets and mechanisms remain unclear. This study investigated whether Ger protects against DKD by modulating podocyte pyroptosis and explored the underlying mechanism. In vivo, diabetic db/db mice were treated with Ger, with benazepril as a positive control. The effects of Ger on DKD were evaluated by assessing biochemical indices and histopathology. Molecular docking, cellular thermal shift assay (CETSA), and drug affinity responsive target stability (DARTS) were employed to assess potential target engagement between Ger and ATP-binding cassette transporter A1 (ABCA1). In vitro, ABCA1 was knocked down in high glucose (HG)-stimulated MPC5 cells, and the effects of Ger were evaluated using the Cell Counting Kit-8, enzyme-linked immunosorbent assay, flow cytometry, and Western blot. Ger reduced fasting blood glucose, improved renal function and alleviated renal pathological injury in db/db mice. Molecular docking, CETSA, and DARTS revealed potential target engagement between Ger and ABCA1. Ger increased ABCA1 mRNA and protein levels, enhanced cholesterol efflux, reduced proinflammatory factor release, and suppressed pyroptosis in db/db mice and HG-stimulated MPC5 cells. ABCA1 knockdown weakened the protective effects of Ger, whereas toll-like receptor 4 (TLR4) inhibition partially reversed the adverse effects of ABCA1 knockdown. Ger alleviates DKD-associated podocyte injury by regulating ABCA1 expression and TLR4-associated pyroptosis, supporting its further evaluation as a therapeutic candidate for DKD.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149293832","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":"Primary cilia dysfunction in nephronophthisis: molecular drivers of pediatric kidney fibrosis and cystogenesis","authors":"Jashan Jindal,&nbsp;Mohd Haneef,&nbsp;Sourabh Kosey,&nbsp;Nanak Singh Toor","doi":"10.1007/s10735-026-11028-2","DOIUrl":"10.1007/s10735-026-11028-2","url":null,"abstract":"<div><p>Nephronophthisis (NPHP) is an inherited autosomal recessive kidney disease in children and adolescents and a major genetic cause of end-stage kidney disease. It is characterized by corticomedullary cysts and progressive tubulointerstitial fibrosis. NPHP is a ciliopathy characterised by dysfunction of primary cilia, which are essential for tubular integrity, repair, and cellular signalling. Over 20 NPHP gene mutations disrupt nephrocystin proteins concentrated in the primary cilium or centrosome, disrupting key signalling pathways including Wnt, Hedgehog, and mTOR. These abnormalities lead to loss of epithelial polarity, cyst formation, and progressive nephron loss. NPHP clinically manifests as infantile, juvenile or adolescent and can be combined with other multisystem disorders like Joubert and Senior–Løken syndromes. This review summarises the clinical spectrum, genetic and molecular mechanisms, diagnostic approaches, emerging gene-based therapies, and future directions for improving the diagnosis and management of NPHP.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149260313","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":"Establishment and evaluation of a rat model of lumbar intervertebral disc degeneration secondary to posterior structural resection","authors":"Dan Wang,&nbsp;Biao Yuan,&nbsp;Lingling Li,&nbsp;Ping Lu,&nbsp;Wu Yang,&nbsp;Qian Wan","doi":"10.1007/s10735-026-11023-7","DOIUrl":"10.1007/s10735-026-11023-7","url":null,"abstract":"<div><p>Intervertebral disc degeneration (IDD) is linked to abnormal mechanical loading. This study investigated early pathological changes in the subchondral bone microenvironment following mechanical destabilization and explored underlying mechanisms. Thirty-six Sprague-Dawley (SD) rats were divided into Control, Sham-operated, and Model groups. The Model group underwent resection of posterior spinal structures (L1–L6) to induce lumbar instability. Multimodal analyses were performed at 4, 8, and 12 weeks postoperatively, including micro-computed tomography (micro-CT) imaging, histopathological staining, serum enzyme-linked immunosorbent assay (ELISA) for inflammatory cytokines, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and reverse transcription-polymerase chain reaction (RT-PCR) for apoptosis-related genes. The Model group demonstrated significant disc height loss, deterioration of subchondral bone microstructure characterized by reduced bone volume fraction, trabecular thickness, trabecular number, and bone mineral density, along with altered trabecular separation. Progressive degradation of the disc matrix was also observed. Concurrently, elevated systemic levels of IL‑6, TNF‑α, and IL‑1β, increased apoptotic cells in subchondral bone, and dysregulated expression of Bax, Caspase‑3, and Bcl‑2 were observed in the Model group. Posterior lumbar instability successfully induced IDD accompanied by significant subchondral bone impairment. Microstructural decay and apoptosis in the subchondral bone were closely associated with disc degeneration, suggesting its potential involvement in mechanically induced IDD and highlighting the bone‑disc interface as a promising therapeutic target.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149260347","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":"Pharmacological modulation of STING-associated signaling alleviates bladder inflammation, epithelial barrier dysfunction, and pain in experimental cystitis","authors":"Chiao-Ching Li,&nbsp;Yi-Hao Lo,&nbsp;Hsiang-Ting Tung,&nbsp;Lun Kelvin Tsou,&nbsp;Ping-Jyun Sung,&nbsp;Mingzi M. Zhang,&nbsp;Chun‑Sung Sung,&nbsp;Zong-Sheng Wu,&nbsp;Zhi-Hong Wen","doi":"10.1007/s10735-026-11006-8","DOIUrl":"10.1007/s10735-026-11006-8","url":null,"abstract":"<div><p>Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic inflammatory disorder characterized by urothelial barrier disruption, neurogenic inflammation, and persistent pelvic pain. However, the upstream molecular mechanisms linking epithelial dysfunction with inflammatory and vascular alterations remain incompletely understood. In this study, we investigated the involvement of STING-associated signaling in experimental cystitis and evaluated the therapeutic potential of the anti-inflammatory marine-derived briareane diterpenoid excavatolide B (EXCB) and its derivative EXCB79 in a cyclophosphamide (CYP)-induced rat model. CYP-induced cystitis was accompanied by increased immunoreactivity of STING together with elevated TBK1 and NF-κB immunostaining, urothelial barrier disruption, CD11b⁺ myeloid cell infiltration, increased expression of the inflammatory mediators COX-2 and IL-1β, angiogenesis-associated changes, and enhanced pelvic hypersensitivity. At the concentrations selected for subsequent analyses, EXCB (20 µg/mL) and EXCB79 (5 µg/mL) attenuated pelvic hypersensitivity and were associated with reduced bladder inflammation and partial preservation of epithelial barrier integrity. Double immunofluorescence analysis demonstrated altered spatial associations between STING and CD11b, CD31, VEGF, ZO-1, E-cadherin, and vimentin following CYP administration. Pharmacological modulation of STING-associated signaling was accompanied by reduced immunoreactivity of STING-associated markers together with attenuation of inflammatory, vascular, and epithelial barrier-related alterations, including reduced VEGF immunoreactivity. Collectively, these findings support an association between STING-associated signaling and inflammatory, vascular, and epithelial alterations in experimental cystitis and suggest that pharmacological modulation of this pathway may represent a potential therapeutic strategy for bladder inflammation and pain-related symptoms.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149260353","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":"Chia seed oil attenuates titanium dioxide nanoparticles-induced ulcerative colitis in rats through suppression of NLRP3 inflammasome pathway “Histological and Molecular Study”","authors":"Nahla Reda Sarhan,&nbsp;Amira I. Shrief,&nbsp;Rasha Elmowafy,&nbsp;Sally A. Elekhtiar","doi":"10.1007/s10735-026-11007-7","DOIUrl":"10.1007/s10735-026-11007-7","url":null,"abstract":"<div><p>Ulcerative colitis (UC) is a chronic inflammatory bowel disease. Titanium dioxide nanoparticles (TiO₂ NPs) are used as a whitening agent in food industry and considered a risk factor for UC. Chia seed oil is nutrient-rich oil with antioxidant and anti-inflammatory properties. NOD-like receptor pyrin domain-containing protein 3 (NLRP3) detects danger signals forming NLRP3 inflammasome complex. This study assessed the attenuating effect of chia seed oil against TiO₂ NPs-induced UC. Forty-eight adult male rats were divided into 4 groups; control, chia: received oral chia seed oil (2.5 ml/kg/day) for 3 weeks, TiO₂: received TiO₂ NPs (100 mg/kg) orally for 2 weeks and TiO₂+chia group: received chia seed oil for 1 week before TiO₂ NPs and continued for 2 weeks. Colon specimens were dissected out for histological and molecular analysis (RT-qPCR) and evaluation of oxidative stress. Serum level of inflammatory cytokines was also measured. Compared to TiO₂ group, TiO₂+chia group showed amelioration of histological changes as preservation of crypts and goblet cell number, attenuation of inflammation, maintenance of junctions, decreased percentage area of fibrosis, Bax, interleukin-1β and proliferating cell nuclear antigen immunostaining. Together with reduced lipid peroxidation, enhanced antioxidant enzymes, downregulation of NLRP3, caspase-1 and interleukin-1β gene expression and reduction of serum inflammatory cytokines. In conclusion, chia seed oil attenuates TiO₂ NPs-induced UC damage through reduction of oxidative stress, downregulation of NLRP3 inflammasome pathway, altered pro-apoptotic signaling, inhibition of fibrosis and cell proliferation; and epithelial barrier preservation. So, it could serve as a prophylactic agent or adjuvant therapy for UC.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149235142","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":"Comprehensive insight into the anti-dyslipidemic and pancreatic lipase inhibition activities of Clematis flammula L. and Fraxinus angustifolia Vahl. extracts using two animal models","authors":"Adlane Zaidi,&nbsp;Dina Atmani-Kilani,&nbsp;Djebbar Atmani,&nbsp;Kenza Moulaoui,&nbsp;Naima Saidene,&nbsp;Nassima Chaher-Bazizi","doi":"10.1007/s10735-026-11011-x","DOIUrl":"10.1007/s10735-026-11011-x","url":null,"abstract":"<div><p><i>Clematis flammula</i> and <i>Fraxinus angustifolia</i> leaves are commonly used in Algeria to treat inflammatory diseases, with potential hypolipidemic effects that have not been investigated so far. The present study explored the in vitro, ex vivo, and in vivo hypolipidemic effects of ethanolic leaf extracts from both plants using two animal models (mice and rabbits) with distinct lipid metabolism. Dyslipidemia was induced by oral administration of Triton X-100, once daily for three consecutive days. Immediately after each Triton X-100 administration, animals received plant extracts (100 and 200 mg/kg bw) or atorvastatin (10 mg/kg bw). Anti-lipase and anti-HMG-CoA reductase activities were evaluated using in vitro and ex vivo assays. Triton X-100 induced marked alterations in serum lipid profiles, characterized by increased LDL-C, VLDL-C, and total cholesterol levels, which were improved by <i>C. flammula</i> and <i>F. angustifolia</i> extracts, particularly at 200 mg/kg bw. While <i>F. angustifolia</i> exhibited greater hypolipidemic efficacy, the lack of improvement in total cholesterol in mice treated with <i>C. flammula</i>, in contrast to rabbits, may suggest species-dependent differences in lipid metabolism, potentially involving CETP-mediated cholesterol transport, which requires further experimental confirmation. In vitro anti-lipase assays showed greater inhibitory potency for <i>F. angustifolia</i> (IC50 = 3.55 µg/mL) than <i>C. flammula</i> (IC50 = 12.10 µg/mL). Both extracts inhibited HMG-CoA reductase activity by over 60% in vitro and ex vivo, with IC50 values of 90.06 and 96.57 µg/mL for <i>F. angustifolia</i> and <i>C. flammula</i>, respectively. Histological examination further supported the hypolipidemic effects of both extracts. Overall, these findings highlight <i>C. flammula</i> and <i>F. angustifolia</i> as promising natural sources of bioactive compounds with potential applications in managing hypercholesterolemia and dyslipidemia.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149234895","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}