Folia Biologica最新文献_第4页

The Potential Inflammatory Role of IL-6 Signalling in Perturbing the Energy Metabolism Function by Stimulating the Akt-mTOR Pathway in Jurkat T Cells. IL-6信号在Jurkat T细胞中通过刺激Akt-mTOR通路干扰能量代谢功能的潜在炎症作用

IF 1.1 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025071010008

Abdullah Alghamdi, Mohammed Alissa

{"title":"The Potential Inflammatory Role of IL-6 Signalling in Perturbing the Energy Metabolism Function by Stimulating the Akt-mTOR Pathway in Jurkat T Cells.","authors":"Abdullah Alghamdi, Mohammed Alissa","doi":"10.14712/fb2025071010008","DOIUrl":"https://doi.org/10.14712/fb2025071010008","url":null,"abstract":"Numerous studies have reported that increased interleukin 6 (IL-6) and soluble IL-6 receptor (sIL-6) levels induce inflammatory conditions. However, the exact mechanisms by which IL-6 drives inflammatory conditions remain unclear. Therefore, we investigated the potential role of IL-6/sIL-6R in inducing energy metabolism, including glycolysis, oxidative phosphorylation, lactate secretion and Akt/mTOR phosphorylation, in Jurkat cells, and whether IL-6 would increase the risk of developing inflammatory conditions due to the high metabolic profile of the T cells. Jurkat CD4 T-cell lines were stimulated with IL-6/sIL-6R for 24 h prior to 48-h stimulation with anti-CD3/CD28. Lactate secretion, glycolysis and oxidative phosphorylation levels were characterized using the Seahorse XF analyser. The Akt and mTOR phosphorylation status was detected using Western blotting. IL-6/sIL-6R significantly induced glycolysis and oxidative phosphorylation and their related parameters, including glycolytic capacity and maximal respiration, followed by significantly increased lactate secretion. Akt and mTOR phosphorylation were increased, which could have resulted from energy metabolism. Here we show that IL-6 enhanced the metabolic profile of Jurkat cells. This effect could have consequences for the metabolism-related signalling pathways, including Akt and mTOR, suggesting that IL-6 might promote T-cell energy metabolism, where T-cell hyperactivity might increase the inflammatory disease risk. The findings should be validated using studies on primary cells isolated from humans.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 1","pages":"8-17"},"PeriodicalIF":1.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144062984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Clinical Value and Regulatory Mechanism of miR-767-5p in Colorectal Cancer. miR-767-5p在结直肠癌中的临床价值及调控机制

IF 1.1 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025071010018

Ping Lin, Xiuju Qin, Caiyun Yi, Man Jiang, Lili Yi, Yuemian Liang

{"title":"Clinical Value and Regulatory Mechanism of miR-767-5p in Colorectal Cancer.","authors":"Ping Lin, Xiuju Qin, Caiyun Yi, Man Jiang, Lili Yi, Yuemian Liang","doi":"10.14712/fb2025071010018","DOIUrl":"https://doi.org/10.14712/fb2025071010018","url":null,"abstract":"The poor prognosis of colorectal cancer (CRC) contributes to a yearly increase in CRC mortality, while microRNAs (miRNAs) were found to play a regulatory function in diversiform cancers, including CRC. The objective of this research was to evaluate the clinical value and possible regulatory mechanisms of miR-767-5p in CRC. The expression level of miR-767-5p in CRC tissues and cells was examined. The Kaplan-Meier curve was utilized to analyse the function of miR-767-5p in CRC prognosis. The independent prognostic factors in CRC were assessed by a multivariate COX regression analysis. Additionally, the regulatory mechanism of miR-767-5p in CRC was determined through an in vitro cell experiment. The miR-767-5p expression was down-regulated in CRC tumour tissues and CRC cells. Indicators such as tumour differentiation, TNM, LNM and miR-767-5p were identified as independent prognostic factors for a poor CRC prognosis. The regulatory relationship between miR-767-5p and nuclear factor I A (NFIA) was verified by the dual-luciferase reporter assay, and the NFIA expression level was significantly suppressed by over-expressed miR-767-5p. The proliferation, migration and invasion of CRC cells were inhibited by over-expressing miR-767-5p, while the inhibition effect could be reversed by over-expressing NFIA. The over-expressed miR-767-5p could serve as a tumour suppressor to inhibit the progression of CRC by suppressing the expression level of NFIA.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 1","pages":"18-28"},"PeriodicalIF":1.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144001705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Comprehensive Analysis of Hub Telomere-Related Genes and Synovial Immune Characteristics in Osteoarthritis. 骨关节炎中心端粒相关基因与滑膜免疫特征的综合分析。

IF 0.6 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025071030123

Chunxiao Du, Weidan Xu

{"title":"Comprehensive Analysis of Hub Telomere-Related Genes and Synovial Immune Characteristics in Osteoarthritis.","authors":"Chunxiao Du, Weidan Xu","doi":"10.14712/fb2025071030123","DOIUrl":"https://doi.org/10.14712/fb2025071030123","url":null,"abstract":"Osteoarthritis (OA) is a degenerative arthritis associated with aging. It is recognized that telomere attrition is a hallmark of aging. However, the transcriptional dynamics of synovial telomere-related genes (TRGs) in OA has not yet been elucidated. OA synovium microarray profiles were sourced from GEO and TRGs from TelNet. GO, KEGG, DO and GSVA enrichment analyses were employed to explore the underlying mechanisms. WGCNA and machine learning methods were utilized to screen hub differentially expressed TRGs (TRDEGs) that highly correlated with OA traits (hub OA-TRDEGs). Nomograms and receiver operating characteristic (ROC) curves were used to evaluate the diagnostic performance of hub OA-TRDEGs. An RNA-binding protein (RBP) network was developed to predict potential RBP target genes. The CIBERSORT analysis was performed to assess associations between hub OA-TRDEGs and immune infiltration. We identified 77 TRDEGs in normal and OA synovium samples. Functional enrichment analysis implicated these ge-nes primarily in metabolism regulation, DNA repair and inflammatory response. LTA4H, HNMT, ANKMY2, UFSP2, HLTF and RPA3 were established as hub OA-TRDEGs, demonstrating strong diagnostic performance for OA. Wilcox testing confirmed significant up-regulation of all hub OA-TRDEGs in OA synovium - a finding validated through independent datasets and qRT-PCR assays. Immune infiltration analysis further indicated that resting mast cells, CD4+ memory resting T cells and activated mast cells are implicated in OA pathogenesis and exhibit significant correlations with hub OA-TRDEGs. These results nominate hub OA-TRDEGs as potential dia-gnostic biomarkers and underscore immune cell infiltration as a critical driver of OA progression.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 3","pages":"123-139"},"PeriodicalIF":0.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145400308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

miR-296-3p Controls Osteogenic Proliferation and Differentiation by Targeting ICAT and Is Involved in Fracture Healing. miR-296-3p通过靶向ICAT调控成骨增殖和分化并参与骨折愈合。

IF 1.1 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025071020064

Feng Xu, Kun Huang, Wenjun Ji, Miao Huang, Jincheng Sima, Jin Li, Hao Song, Wei Xiong, Zhong Tian

{"title":"miR-296-3p Controls Osteogenic Proliferation and Differentiation by Targeting ICAT and Is Involved in Fracture Healing.","authors":"Feng Xu, Kun Huang, Wenjun Ji, Miao Huang, Jincheng Sima, Jin Li, Hao Song, Wei Xiong, Zhong Tian","doi":"10.14712/fb2025071020064","DOIUrl":"https://doi.org/10.14712/fb2025071020064","url":null,"abstract":"Fragility fractures have been a cause for concern because of their high incidence. For the prevention and treatment of osteoporotic fractures, it is important to understand how to promote bone formation and increase bone mass. This study investigated miR-296-3p expression and function in fragility fracture. The study enrolled 98 patients with hip fractures, 90 patients with wrist fractures and 35 healthy controls. RT-qPCR was used to detect the miR-296-3p level changes before and after surgery in fracture patients and during the differentiation of human bone mesenchymal stem cells (BMSCs). The starBase bioinformatics database was used for prediction of the miR-296-3p target gene, and dual luciferase report was used for verification of the target relationship. Our results demonstrated that miR-296-3p levels are up-regulated in fracture patients, while they gradually decrease during human BMSC differentiation. The up-regulation of miR-296-3p inhibited the proliferation and differentiation ability of human BMSCs, while inhibition of its expression had the opposite effects. miR-296-3p negatively regulates osteogenic differentiation, and over-expression of inhibitor of β-catenin and TCF (ICAT) could counteract the negative regulatory effect. miR-296-3p targets ICAT and affects the expression of key proteins in the Wnt/β-catenin signalling pathway. In conclusion, miR-296-3p can regulate the division and differentiation of osteoblasts by affecting the expression of ICAT and participate in fracture healing.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 2","pages":"64-72"},"PeriodicalIF":1.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

miR-4478 Promotes Ferroptosis of Nucleus Pulposus Cells through Targeting SLC7A11 to Induce IVDD. miR-4478通过靶向SLC7A11诱导IVDD促进髓核细胞铁下垂。

IF 1.1 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025071010029

Dongliang Gong, Long Jia, Yuhang Wang, Chengwei Xu, Xuxing Sun, Xiao Wu, Xiaojun Han

{"title":"miR-4478 Promotes Ferroptosis of Nucleus Pulposus Cells through Targeting SLC7A11 to Induce IVDD.","authors":"Dongliang Gong, Long Jia, Yuhang Wang, Chengwei Xu, Xuxing Sun, Xiao Wu, Xiaojun Han","doi":"10.14712/fb2025071010029","DOIUrl":"https://doi.org/10.14712/fb2025071010029","url":null,"abstract":"Nucleus pulposus cells (NPC) are important for the development of intervertebral disc degeneration (IVDD). miR-4478 can aggravate IVDD, but whether it can aggravate IVDD by regulating ferroptosis in NPC remains unclear. The optimal level of ferroptosis activator RSL3 for eliciting ferroptosis in NPC was screened by Western blot and CCK-8 assay. The targeting relationship between miR-4478 and its potential target solute carrier family 7 member 11 (SLC7A11) was explored based on dual luciferase assay. On this basis, IVDD models were constructed. After over-expression or knockdown of miR-4478 or SLC7A11, CCK-8 and calcein-AM/PI assays were employed to evaluate cell damage. Flow cytometry, Western blot and Prussian blue staining were employed to evaluate oxidation and ferroptosis levels, and histopathological staining was applied to evaluate the intervertebral disc tissue injury degree. The optimal concentration of RSL3 was 1 μM. Under these conditions, miR-4478 or SLC7A11 can be effectively over-expressed or knocked down after transfection. Knockdown of miR-4478 can improve the survival rate of NPC, the level of Fe2+ ions, improve the pathological damage of intervertebral disc structure, reduce iron deposition in tissues, and significantly reduce expression of reactive oxygen species (ROS) and ferroptosis-related protein. The levels of antioxidant enzymes were significantly increased. When miR-4478 was over-expressed, the above phenomenon was reversed. On this basis, after SLC7A11 was over-expressed, the effect of miR-4478 up-regulation was weakened, and NPC ferroptosis was improved. miR-4478 can target SLC7A11 to promote NPC damage, peroxide accumulation and iron metabolism disorders, leading to ferroptosis, thereby inducing IVDD.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 1","pages":"29-43"},"PeriodicalIF":1.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144001827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PCAT7 Enhances Doxorubicin Resistance of Osteosarcoma by Modulating TGF-β Signalling. PCAT7通过调节TGF-β信号传导增强骨肉瘤阿霉素耐药性

IF 0.6 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025.0003

Bin Fang, Yongde Chen, Zi Li, Haitao Sun, Sheng Wei

{"title":"PCAT7 Enhances Doxorubicin Resistance of Osteosarcoma by Modulating TGF-β Signalling.","authors":"Bin Fang, Yongde Chen, Zi Li, Haitao Sun, Sheng Wei","doi":"10.14712/fb2025.0003","DOIUrl":"https://doi.org/10.14712/fb2025.0003","url":null,"abstract":"Long noncoding RNAs (lncRNAs) are known to play critical roles in the progression of osteosarcoma. Despite their recognized importance, the specific biological functions of lncRNAs in osteosarcoma remain unclear. In this context, prostate cancer-associated transcript 7 (PCAT7) has been identified as a bone metastasis-related lncRNA through the analysis of The Cancer Genome Atlas dataset. In this study, we investigated the expression of PCAT7 in osteosarcoma cells, particularly those exhibiting resistance to doxorubicin, a widely used chemotherapeutic agent in clinic. Functional assays including cell growth, invasion and apoptosis were conducted to elucidate the impact of PCAT7 inhibition on osteosarcoma cells, focusing on sensitivity to doxorubicin treatment. To understand the underlying molecular mechanisms, the interaction between PCAT7, miR-324-5p, and the TGF-β/SMAD signalling pathway was further explored. The study revealed that PCAT7 is up-regulated in osteosarcoma cells with doxorubicin resistance. Inhibition of PCAT7 could enhance the sensitivity to doxorubicin treatment by reducing cell growth, suppressing cell invasion and increasing cell apoptosis. Mechanistically, PCAT7 was shown to activate the TGF-β/SMAD signalling pathway by up-regulating the expression of TGFBR1 through sponging miR-324-5p. These findings unveil a novel mechanism contributing to the constitutive activation of TGF-β signalling in osteosarcoma. Targeting PCAT7 may offer a promising avenue for therapeutic interventions in osteosarcoma by disrupting the aberrant TGF-β signalling, thus presenting a potential strategy to improve treatment outcomes in this challenging cancer.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 4","pages":"171-179"},"PeriodicalIF":0.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145862493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Endothelium and Systemic Inflammation in Neonates and Children. 新生儿和儿童的内皮和全身性炎症。

IF 1.1 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025071020055

Petr Janec, Jana Dorňáková, Jan Živný, Jan Janota

引用次数: 0

Atractylenolide III Promotes Astrocyte Aβ Clearance by Up-regulating AQP4 to Improve Alzheimer's Disease. 苍术内酯III通过上调AQP4促进星形细胞Aβ清除，改善阿尔茨海默病。

IF 0.6 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025071030140

Jingwen Hao, Qi Wan, Chanjuan Chen

{"title":"Atractylenolide III Promotes Astrocyte Aβ Clearance by Up-regulating AQP4 to Improve Alzheimer's Disease.","authors":"Jingwen Hao, Qi Wan, Chanjuan Chen","doi":"10.14712/fb2025071030140","DOIUrl":"https://doi.org/10.14712/fb2025071030140","url":null,"abstract":"Astrocytes actively phagocytose amyloid beta (Aβ), enhancing cerebral clearance and positioning themselves as viable therapeutic targets for Alz-heimer's disease (AD). Atractylenolide III (ATL-III), the primary bioactive compound in the traditional Chinese herb Baizhu, demonstrates established neuroprotective properties. However, the research on its effects on astrocytes has not yet been elaborated. To induce an astrocyte-based AD model, Aβ1-42 was utilized. Cell viability assays were conducted to screen for the optimal concentration of ATL-III treatment. Molecular docking was performed to investigate the binding between ATL-III and aquaporin 4 (AQP4). Additionally, an Aβ1-42-induced AD mouse model was adopted. In this study, ATL-III effectively reduced the accumulation level of Aβ1-42 in the cell supernatant, and at the same time, significantly enhanced the internalization of Aβ by astrocytes. Of interest, the study reveals that ATL-III not only has the property of binding to AQP4 but also up-regulates the expression level of this protein. Mechanistic probes suggest that the role of ATL-III in promoting Aβ clearance by astrocytes may be partially dependent on its regulation of AQP4 expression. Animal behavioural experiments confirmed that the compound ameliorated Aβ1-42-induced cognitive dysfunction, and pathological analyses revealed significantly elevated AQP4 expression in the hippocampus. The combined findings suggest that ATL-III may play a role in ameliorating the pathological process of AD by enhancing the efficiency of astrocyte-mediated Aβ clearance through the up-regulation of AQP4 expression.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 3","pages":"140-148"},"PeriodicalIF":0.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145400251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exploring IDH1 and IDH2 Mutations in Paediatric Medulloblastoma. 探讨儿童髓母细胞瘤中IDH1和IDH2突变。

IF 1.1 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025071020073

Motaz Fadul, Saleh Baeesa, Alaa Alkhotani, Amany A Fathaddin, Ahmed I Lary, Bassam Addass, Taghreed Alsinani, Ahmed Bamaga, Ahmad Albeshri, Mohammed M Karami, Mohammed A Abutalib, Maher Kurdi

{"title":"Exploring IDH1 and IDH2 Mutations in Paediatric Medulloblastoma.","authors":"Motaz Fadul, Saleh Baeesa, Alaa Alkhotani, Amany A Fathaddin, Ahmed I Lary, Bassam Addass, Taghreed Alsinani, Ahmed Bamaga, Ahmad Albeshri, Mohammed M Karami, Mohammed A Abutalib, Maher Kurdi","doi":"10.14712/fb2025071020073","DOIUrl":"https://doi.org/10.14712/fb2025071020073","url":null,"abstract":"Medulloblastoma (MB) in children is associated with distinct molecular subgroups, reflecting substantial biological heterogeneity. The presence of isocitrate dehydrogenase 1 (IDH1) and IDH2 mutations in paediatric MB has been rarely reported and not routinely investigated. Our study included 23 samples from paediatric patients diagnosed with MB. Hotspot alterations at codons IDH1 R132 and IDH2 R172 were examined using Sanger sequencing following polymerase chain reaction (PCR). The mean age of the patients was 10 years (SD: 4.25), comprising 17 males and 6 females. All cases exhibited classical histological features of MB. β-Catenin expression was observed in four cases (17.4 %), while 19 cases (82.6 %) showed no expression. No statistically significant differences in progression-free survival (PFS) were found between MBs with positive or negative β-catenin expression (P = 0.6). Radiotherapy alone was administered to four patients (17.4 %), while 19 patients (82.6 %) received combined radiotherapy and chemotherapy. The median PFS was 383 days (1 year and 18 days). IDH1 R132 or IDH2 R172 hotspot mutations were not detected in any of the samples. The absence of IDH1 or IDH2 mutations in paediatric MB may be attributed to differences in mutational profiles and cellular origins in childhood MB, despite its histomolecular similarities with adult MB.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 2","pages":"73-78"},"PeriodicalIF":1.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effect of Zoledronic Acid on the Femoral Bone Morphology and Innervation in Rats with Glucocorticoid-Induced Osteoporosis. 唑来膦酸对糖皮质激素所致骨质疏松大鼠股骨形态及神经支配的影响。

IF 1.8 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025.0005

Nazar M Kostyshyn, Ewa Tomaszewska, Siemowit Muszyński, Marcin B Arciszewski, Maria Mielnik-Błaszczak, Damian Kuc, Piotr Dobrowolski

{"title":"Effect of Zoledronic Acid on the Femoral Bone Morphology and Innervation in Rats with Glucocorticoid-Induced Osteoporosis.","authors":"Nazar M Kostyshyn, Ewa Tomaszewska, Siemowit Muszyński, Marcin B Arciszewski, Maria Mielnik-Błaszczak, Damian Kuc, Piotr Dobrowolski","doi":"10.14712/fb2025.0005","DOIUrl":"10.14712/fb2025.0005","url":null,"abstract":"Long-term glucocorticoid therapy, commonly used because of its potent anti-inflammatory effects, frequently leads to glucocorticoid-induced osteoporosis (GIOP), causing severe bone loss and increased fracture risk. Given the limited effectiveness of current therapies in addressing both bone structural deterioration and impaired bone innervation, we evaluated whether low-dose zoledronic acid (ZOL) could alleviate these detrimental effects on bone architecture and neural integrity in a rat model of GIOP. Thirty-six male Wistar rats were divided into three groups: control (saline), glucocorticoid-treated (methylprednisolone, 3 mg/kg every other day) and glucocorticoid-ZOL-treated (0.025 mg/kg monthly). After 8 and 16 weeks, comprehensive histological and immunohistochemical analyses were performed to assess bone morphology, the expression of osteocalcin (OC), osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-B ligand (RANKL), as well as neural integrity using markers vasoactive intestinal polypeptide (VIP) and protein gene product 9.5 (PGP9.5). Glucocorticoid treatment significantly increased cytokine responses at trabecular bone surfaces, indicating accelerated remodelling and structural deterioration. It also adversely affected the neuronal morphology and distribution within the femoral bone. ZOL partially mitigated glucocorticoid-induced bone structural impairments, significantly reducing trabecular bone loss and remodelling disturbances. Importantly, ZOL did not exacerbate the glucocorticoid-induced neuronal alterations. We conclude that low-dose periodic administration of ZOL effectively reduces glucocorticoid-induced structural deterioration of the femoral bone without negatively influencing neuronal integrity. These findings support ZOL as a potential therapeutic strategy for simultaneously preserving bone health and neural function in glucocorticoid-induced osteoporosis.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 5-6","pages":"193-211"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147289724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0