Folia histochemica et cytobiologica最新文献

{"title":"Aggressiveness of papillary thyroid carcinoma: a comprehensive analysis from molecular mechanisms to clinical applications.","authors":"Min Wang, Bin Li","doi":"10.5603/fhc.108530","DOIUrl":"10.5603/fhc.108530","url":null,"abstract":"<p><p>Papillary thyroid carcinoma (PTC) constitutes the predominant subtype among thyroid malignancies. Despite its generally favorable prognosis, certain aggressive subtypes, along with recurrent and metastatic manifestations, substantially affect patient survival outcomes. Recent advancementsin the diagnostic and therapeutic strategies for PTC have ushered in a new era, characterized by the integration of molecular mechanisms and imaging-based evaluations. This review offers an integrated perspective of the clinicopathological features, molecular genetic characteristics, epigenetic regulation, and the contribution of the immune microenvironment to the aggressiveness of PTC. Primary inve stigation targets include BRAF/RAS/RET-related molecular mechanisms and the functional significance of non-coding RNAs [especially long non-coding RNAs (lncRNAs) and microRNAs (miRNAs)] in molecular regulation. Additionally, the impact of clinical factors such as age, sex, obesity, and comorbidity with Hashimoto's thyroiditis on the aggressiveness of PTC is thoroughly examined. Furthermore, this review systematically synthesizes the clinical advances in the early detection and risk assessment of aggressive PTC by emerging imaging modalities such as conventional ultrasound, interventional ultrasound, ultrasound elastography, contrast-enhanced ultrasound, and artificial intelligence-assisted analysis. Looking ahead, multidisciplinary collaborations integrating pathology, genomics, and imaging are anticipated to enhance the precise evaluation of PTC aggressiveness and facilitate the development of individualized treatment strategies. This review serves as a comprehensive reference for mechanistic exploration and clinical translation in the study of PTC aggressiveness, and provides guidance for the progression of precision medicine and management models for PTC patients.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"99-112"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145285977","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":"A recombinase polymerase amplification-coupled Cas12a for detection of Salmonella Typhi - a preliminary report.","authors":"Qian Dong, Chujun Luo","doi":"10.5603/fhc.108406","DOIUrl":"https://doi.org/10.5603/fhc.108406","url":null,"abstract":"<p><strong>Introduction: </strong>. Typhoid fever, a disease resulting from an infection with Salmonella Typhi (S. Typhi) remains widespread in economically disadvantaged regions, where it continues to be a critical public health concern. As the symptoms and signs are non-specific, they are difficult to diagnose directly based on the clinical picture. Therefore, laboratory examinations are essential for diagnosis.</p><p><strong>Material and methods: </strong>. This research introduces a fast and equipment-independent approach for detecting S. Typhi by employing CRISPR/Cas12a-based technology. The optimized CRISPR/Cas12a system achieved a detection limit of 103 copies/μL of S. Typhi DNA per reaction, with the entire assay completed within 60 min.</p><p><strong>Results: </strong>. Four clinical isolates cultured from patients with typhoid fever were collected and evaluated using our CRISPR/Cas12a-based detection system. The assay results demonstrated that all four samples were accurately identified as positive.</p><p><strong>Conclusions: </strong>. We showed that the developed CRISPR/Cas12a-based detection method provides a promising alternative for the on-site and simple detection of S. Typhi.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"63 4","pages":"185-192"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145959035","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":"Mechanisms of alleviating sepsis-induced rat lung and kidney damage by inhibiting expression of miRNA-939.","authors":"Anwaier Apizi, Jian Li, Yan Li, Zhaoxia Yu, Ruifeng Chai","doi":"10.5603/fhc.101988","DOIUrl":"10.5603/fhc.101988","url":null,"abstract":"<p><strong>Introduction: </strong>Sepsis, a life-threatening condition caused by a host response that goes out of control, leads to severe organ dysfunction. MicroRNA 939 (miRNA-939) plays a pivotal role in this process by post-transcriptionally regulating the mRNA expression of key enzymes in the NO/cGMP pathway. This pathway is crucial in the development of refractory hypotension and organ failure in sepsis. The aim of the study was to explore the effects of miRNA-939 on a caecum ligation puncture (CLP) rat model of sepsis in kidneys and lungs in order to elucidate its role in modulating the NO/cGMP pathway and related organ protection mechanisms.</p><p><strong>Material and methods: </strong>To explore the effects of miRNA-939 on sepsis, three groups of rats were established: a sham surgery group, a sepsis model group, and an intervention group treated with LNA-antimiR targeting miRNA-939, which was administered via tail vein injection (the locked nucleic acid (LNA) group). miRNA-939 levels in serum, kidneys, and lungs were assessed using reverse transcription-polymerase chain reaction (RT-PCR). The protein levels of inducible nitric oxide synthase (iNOS) and soluble guanylate cyclase (sGC) were quantified using Western blotting. Serum nitric oxide (NO) levels were determined using the nitrate reductase method.</p><p><strong>Results: </strong>Compared to the sham group, the rats in the sepsis model group exhibited significantly elevated levels of miRNA-939 in serum, with distinct peaks at 12, 24, and 36 h post-sepsis induction. Similarly, the protein levels of iNOS and sGC (sGCα1 and sGCβ1 subunits) in kidneys and lungs were markedly higher in the sepsis group. Serum NO levels were also significantly elevated in the sepsis group compared to the sham group. Importantly, inhibition of miRNA-939 in the LNA group led to a significant reduction in the tissue levels of iNOS, sGCα1, sGCβ1, and serum NO within the NO/cGMP pathway, alongside mitigating inflammatory damage to kidneys and lungs.</p><p><strong>Conclusions: </strong>Inhibiting miRNA-939 significantly reduces the expression of iNOS, sGCα1, sGCβ1, and NO in the NO/cGMP pathway in CLP-exposed rats, thereby alleviating inflammatory organ damage in sepsis. These findings highlight the therapeutic potential of targeting miRNA-939 in the management of sepsis-induced organ dysfunction.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"88-98"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150002","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":"Electroacupuncture ameliorates depressive-like behaviors by activating Sirt1 to enhance oligodendrocyte differentiation and myelination in the prefrontal cortex of rats.","authors":"Hui-Qian Cai, Tian Wang, Li-Xia Lin, Xin Li, Guang-Mei Zheng, Sheng-Yong Su","doi":"10.5603/fhc.106467","DOIUrl":"10.5603/fhc.106467","url":null,"abstract":"<p><strong>Introduction: </strong>This study investigated the therapeutic mechanisms of electroacupuncture (EA) in chronic unpredictable stress (CUS)-induced depression rat model. Since SIRT1 plays in oligodendrocyte differentiation and neuroprotection, we hypothesize that it may mediate the effect of electroacupuncture (EA) on myelin regeneration in depression.</p><p><strong>Material and methods: </strong>Sixty adult male Sprague-Dawley rats were divided into control, CUS, EA + CUS and CUS + EA + SIRT1-specific inhibitor - EX527 (EX) groups. We established a CUS-induced depression rat model by subjecting rats to 4-week CUS paradigm. Four weeks post-modeling, EA treatment and intraperitoneal administration of EX527 were applied. Behavioral tests including open field test, forced swim test and sucrose preference test were performed to assess the depressive-like state. Immunohistochemistry and stereological analysis for quantification of oligodendroglial cell populations was performed. Immunohistochemical staining and transmission electron microscope were performed for evaluation of myelination. Western blot and qRT-PCR analyses were performed to detect the mRNA and protein expression of SIRT1 in the prefrontal cortex (PFC) of rats in each group.</p><p><strong>Results: </strong>Four weeks of EA intervention significantly alleviated depressive-like behaviors in CUS rats, as evidenced by increased sucrose preference (P < 0.05), enhanced exploratory activity (P < 0.01), and reduced immobility time (P < 0.05) compared to the CUS group. Histopathological and ultrastructural analyses demonstrated that EA restored myelin integrity in the PFC, with myelin basic protein immunoreactivity significantly higher in the EA+CUS group than in untreated CUS rats (P < 0.05). Electroacupuncture promoted oligodendrocyte differentiation, reversing the chronic stress-induced reduction in CC1+/Olig2+/BrdU+ progenitor cells (31.5 ± 3.1% vs. 3.23 ± 1.4% in CUS + EA + EX group, P < 0.01). Mechanistically, EA upregulated SIRT1 mRNA and protein expression in the PFC (P < 0.05 vs. CUS), while pharmacological inhibition of Sirt1 with EX-527 abolished these effects, reducing Sirt1 mRNA and SIRT1 protein expression (P < 0.01, P < 0.01, respectively) and Olig2 expression (P < 0.05). EX-527 treatment also blocked EA-induced behavioral improvements and myelin regeneration, confirming the critical role of the Sirt1.</p><p><strong>Conclusions: </strong>The findings indicate that EA ameliorates depression-like behavior by enhancing oligodendrocyte maturation and myelin repair via activating SIRT1 signaling. These findings provide novel mechanistic insights into non-pharmacological interventions for depression.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"121-133"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145130463","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":"Genetic alterations in papillary thyroid cancer: clinicopathological correlations and diagnostic implications.","authors":"Enaam Mohammed Ali Junainah","doi":"10.5603/fhc.106400","DOIUrl":"10.5603/fhc.106400","url":null,"abstract":"<p><strong>Introduction: </strong>Papillary thyroid carcinoma (PTC) is the most common thyroid malignancy, encompassing distinct histological variants and a wide spectrum of clinical behaviors. Advances in molecular diagnostics have identified key genetic alterations - particularly BRAFV600E, RAS mutations, RET/PTC fusions, and TERT promoter mutations - that are strongly linked to tumor aggressiveness and prognosis. This study aimed to determine the prevalence of these alterations and evaluate their clinicopathological significance in a Saudi Arabian patient cohort.</p><p><strong>Materials and methods: </strong>A retrospective analysis was conducted on 114 formalin-fixed paraffin-embedded (FFPE) PTC samples diagnosed between 2019 and 2023. Targeted next-generation sequencing (NGS) was used to detect BRAF, NRAS, KRAS, HRAS, RET/PTC fusions, and TERT promoter mutations. Immunohistochemistry (IHC) for BRAFV600E, TTF-1, CK19, HBME-1, and galectin-3 was performed using automated staining systems. Associations between genetic alterations and clinicopathological parameters - including tumor size, histological subtype, lymph node metastasis, and extrathyroidal extension - were analyzed statistically.</p><p><strong>Results: </strong>BRAFV600E mutations were identified in 39.5% of cases and were significantly associated with larger tumor size (P = 0.01), extrathyroidal extension (P = 0.04), and lymph node metastasis (P = 0.03). RET/PTC fusions were detected in 15.8% of patients, predominantly younger individuals, and correlated with multifocal tumors and lymphovascular invasion. RAS mutations (19.3%) were more frequent in the follicular variant but showed no significant association with adverse features. TERT promoter mutations were present in 10.5% of cases, significantly correlating with older age and advanced tumor stage. IHC profiles demonstrated strong concordance with molecular findings.</p><p><strong>Conclusions: </strong>In this Middle Eastern cohort of PTC patients, BRAFV600E and TERT promoter mutations were significantly associated with aggressive clinicopathological features, while RET/PTC fusions and RAS mutations demonstrated distinct demographic and histological distributions. The integration of NGS and IHC enhanced diagnostic accuracy and supports personalized risk stratification in PTC management.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"113-120"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198951","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":"Critical assessment of microscopy methods for detecting single- and double-strand DNA breaks.","authors":"Agnieszka Hoang-Bujnowicz, Julita Wesolowska, Agnieszka Ostromecka, Beata Nosal, Weronika Pawlus, Svitlana Levchenko, Miroslaw Zarebski, Jurek W Dobrucki","doi":"10.5603/fhc.109368","DOIUrl":"10.5603/fhc.109368","url":null,"abstract":"<p><p>A laboratory toolbox for detecting and quantifying DNA breaks in animal cells and tissues includes various methods that employ biochemical tests, DNA sequencing, or imaging approaches. Various methods based on microscopy were developed to detect DNA breaks in fixed and live cells, including the nick translation assay, TUNEL, STRIDE, and detection methods based on imaging of histone modifications (γH2A.X), recruitment of repair factors (XRCC1, PCNA, 53BP1, Rad51) or poly-ADP-ribosylation. This review discusses the advantages and limitations of various microscopy-based methods for the detection and quantification of single- and double-strand DNA breaks.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"151-161"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145586498","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":"Enhanced migration and adhesion protein expression by polyethylene glycol 4-modified SVVYGLR peptide in an in vitro human gingival fibroblast wound healing model.","authors":"Peiying Xiong, Chengcheng Yu, Zhihui Chen, Luyuan Chen, Yonglong Hong, Buling Wu","doi":"10.5603/fhc.104010","DOIUrl":"https://doi.org/10.5603/fhc.104010","url":null,"abstract":"<p><strong>Introduction: </strong>This study was aimed at exploring the effect of four units of polyethylene glycol (PEG4)-modified Ser-Val-Val-Tyr-Gly-Leu-Arg (SVVYGLR) peptide (SV peptide) on the proliferative potential and migrative capability of human gingival fibroblasts (HGFs) and the activation of adhesion-related proteins.</p><p><strong>Material and methods: </strong>PEG4-SV peptide was synthesised using peptide solid phase synthesis. The proliferative response of HGFs to varying concentrations of PEG4-SV peptide was quantitatively evaluated using a Cell Counting Kit-8 (CCK-8) assay. The migratory capacity of HGFs in response to PEG4-SV peptide treatment was evaluated using an in vitro wound healing assay. The expression levels of adhesion-related genes, including collagen type I (COL-1), vinculin (VCL), focal adhesion kinase (FAK), and integrin β1(ITGB1), were quantitatively analysed using qRT-PCR. To assess the aforementioned adhesion-related proteins, immunofluorescence and Western blotting were performed.</p><p><strong>Results: </strong>Primary HGFs were isolated through enzymatic digestion using dispase, and subsequently characterised by positive immunoreactivity for both vimentin and CD90 (Thy-1) markers. Compared to the control group, PEG4-SV at concentrations of 10, 20, and 40 μg/mL significantly promoted the proliferation of HGFs. The wound area in the SV group exhibited a significantly smaller size in the monolayer cell culture at 24 and 48 h. The expression of adhesion-related genes and proteins (collagen type I, vinculin, FAK and integrin β1), were significantly upregulated after treatment with 20 μg/mL PEG4-SV.</p><p><strong>Conclusions: </strong>These results demonstrate that PEG4-SV peptide may have the ability to promote soft tissue healing around an implant surface and form tight soft tissue sealing on the transmucosal part of the implant.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"63 1","pages":"41-50"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149789","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":"Potential O-GlcNAcylation and odontoblast differentiation in dental pulp stem cells.","authors":"María Teresa Hernández-Huerta, Laura Pérez-Campos Mayoral, Hector Alejandro Cabrera-Fuentes, Eduardo Pérez-Campos, Efrén Emmanuel Jarquín González","doi":"10.5603/fhc.107130","DOIUrl":"10.5603/fhc.107130","url":null,"abstract":"","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"149-150"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145130412","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":"Upregulation of SIRT1 ameliorates apoptosis of rat nucleus pulposus cells under oxidative stress through FoxO1/β-catenin pathway.","authors":"Hongtao Hu, Sheng Wang, Haijun Teng, Sishun Zhao, Weisheng Hong","doi":"10.5603/fhc.104395","DOIUrl":"10.5603/fhc.104395","url":null,"abstract":"<p><strong>Introduction: </strong>Age-related degenerative changes in intervertebral discs (IVDs) can lead to lower back pain, and even paralysis. This topic is therefore garnering growing attention in an increasingly ageing society. The oxidative stress-induced degenerative process is a major contributor to apoptosis in nucleus pulposus cells. However, the regulatory mechanism of NAD-dependent protein deacetylase Sirtuin-1 (SIRT1) on apoptosis in oxidative stress-induced rat nucleus pulposus cells remains unclear.</p><p><strong>Material and methods: </strong>Rat nucleus pulposus cells (NPCs) were induced to undergo degenerative changes through H₂O₂ exposure, simulating the ageing oxidative stress process. Subsequently, the SIRT1 activator SRT2104 was employed to explore the impact of SIRT1 on the expression of markers of ageing oxidative stress process in NPCs. The FoxO1 inhibitor AS1842856 was used to investigate the role of the downstream signalling pathway FoxO1/β-catenin in ageing NPCs under the influence of SRT2104. TUNEL staining and other assays such as CCK were used to observe the effects of H₂O₂ on cell apoptosis and viability, respectively. The influence of the aforementioned treatments on the ageing phenotype was observed through β-galactosidase staining, immunofluorescence staining, flow cytometry analysis, and protein electrophoresis.</p><p><strong>Results: </strong>Under H₂O₂-induced oxidative stress, both the mRNA and protein levels of SIRT1 decreased in rat NPCs. Conversely, specific activation of SIRT1 inhibited apoptosis and reduced the expression of senescence-associated secretory phenotype (SASP) and ageing-related proteins. Meanwhile, inhibiting FoxO1 expression with AS1842856 significantly upregulated β-catenin protein levels, suppressing the apoptosis process in ageing NPCs under oxidative stress.</p><p><strong>Conclusions: </strong>These results suggest that activation of the SIRT1/FoxO1/β-catenin axis can diminish ageing-related phenotypes and cell apoptosis in NPCs, inhibiting the oxidative stress-induced ageing process triggered by H₂O₂. These findings may offer a new perspective for the treatment of intervertebral disc degeneration (IDD) in the future.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"53-64"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149835","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":"MiR-494-3p knockdown promotes osteogenic differentiation of bone marrow mesenchymal stem cells in ovariectomised rats by targeting Sirt1/TLR4/NF-κB pathway.","authors":"Jianping Lei, Song Guo, Jiabing Kuang, Bo Shen, Zixi Li","doi":"10.5603/fhc.104450","DOIUrl":"10.5603/fhc.104450","url":null,"abstract":"<p><strong>Introduction: </strong>Osteoporosis is a bone disease characterised by low bone mass, deterioration of bone tissue, and disruption of bone microarchitecture. MicroRNAs have been found to play an important role in osteoporosis. MicroRNA (miR)-494 is inhibited during bone angiogenesis, and its overexpression reduces osteogenic differentiation gene expression. Sirtuin 1 (Sirt1) is a histone deacetylase with multiple cellular activities including increasing bone mass and delaying the onset of osteoporosis. MiR-494-3p has been predicted in computer-assisted bioinformatics analysis to target the 3'UTR of Sirt1 mRNA. The aim of the present study was to assess the effect of miR-494-3p on ovariectomy (OVX)-induced osteoporosis in rats and the relevant mechanisms.</p><p><strong>Material and methods: </strong>Osteoporosis in female rats was induced by OVX, and bone microarchitectural changes were evaluated by means of microCT. MiR-494-3p and Sirt1 expression in femurs were evaluated by RT-qPCR or Western blotting. Bone marrow mesenchymal stem cells (BMSCs) were isolated from rat femurs and identified by flow cytometry. Then, BMSCs were transfected with miR-494-3p inhibitor/mimic, si-Sirt1 and negative controls as well as pcDNA3.1-TLR4 and empty pcDNA3.1 vector. Osteogenic cell differentiation was assessed via Alizarin Red, alkaline phosphatase (ALP) and Oil Red O staining.</p><p><strong>Results: </strong>MiR-494-3p level was upregulated, and Sirt1 mRNA and protein levels were downregulated, in femurs of OVX rats. Functionally, miR-494-3p inhibited osteogenic differentiation of cultured rat BMSCs. Mechanistically, miR-494-3p regulated the Sirt1 3'UTR to activate TLR4/NF-κB signalling, and Sirt1 inhibition and TLR4 overexpression reversed the enhancing effect of miR-494-3p knockdown on osteogenic differentiation.</p><p><strong>Conclusions: </strong>MiR-494-3p represses osteogenic differentiation of BMSCs in OVX rats through Sirt1/TLR4/NF-κB signalling.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"65-78"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149953","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}