Journal of Molecular Histology最新文献

{"title":"FGF5 alleviates ferroptosis in renal tubular epithelial cells by inducing mitophagy under in vitro ischemia–reperfusion-like injury","authors":"Dongxu lin,&nbsp;Tianen Wu,&nbsp;Hongyuan Huang,&nbsp;Xiaoyu Hong","doi":"10.1007/s10735-025-10594-1","DOIUrl":"10.1007/s10735-025-10594-1","url":null,"abstract":"<div><p>Renal ischemic disease represents a severe clinical pathological condition commonly observed in acute kidney injury (AKI), renal transplantation, and kidney surgery. It leads to renal tubular epithelial cell damage, inflammatory responses, and cell death, potentially progressing to chronic kidney disease (CKD) or even renal failure, significantly impairing patients' quality of life and survival rates. Current therapeutic strategies for renal ischemia–reperfusion injury (IRI) include pharmacological interventions, cell therapy, and gene therapy, yet their efficacy remains limited and may be accompanied by adverse effects. Thus, there is an urgent need to explore novel therapeutic targets and strategies. Fibroblast growth factor 5 (FGF5), a key member of the FGF family, plays crucial roles in cell proliferation, differentiation, and tissue repair. However, its specific mechanism in renal IRI remains unclear. This study aimed to investigate the therapeutic effects of FGF5 on renal IRI and its underlying molecular mechanisms in vitro. Using normal rat kidney-52E (NRK-52E) and human kidney-2 (HK-2 cell) models, we evaluated the impact of FGF5 on cell viability, oxidative stress, inflammatory responses, and renal cell death. Our findings demonstrate that FGF5 exhibits significant biological activity and further reveal its regulatory role in suppressing ferroptosis through activation of the Mitophagy. In conclusion, this study identifies FGF5 as a potential therapeutic agent for renal IRI and provides a theoretical foundation for developing FGF5-based treatment strategies. These findings hold substantial scientific and clinical value, potentially opening new avenues for treating renal ischemic diseases.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144998562","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":"Chrysin inhibits hypertrophic scar formation through TGF-β/Smad signaling pathways","authors":"Lingyan Shen,&nbsp;Lin Chen,&nbsp;Jin Yang,&nbsp;Chenhuan Liu,&nbsp;Hongshun Liao,&nbsp;Qin Yu,&nbsp;Xiaoyan Wen,&nbsp;Yafei Yang","doi":"10.1007/s10735-025-10576-3","DOIUrl":"10.1007/s10735-025-10576-3","url":null,"abstract":"<div>\u0000 \u0000 <p>Hypertrophic scar (HS) is a complex fibrotic skin condition characterized primarily by proliferation of abnormal fibroblasts and accumulation of excessive extracellular matrix (ECM). Chrysin (CHR), a naturally occurring flavonoid compound, has been shown to exhibit anti-fibrotic properties in multiple disease models. The aim of this study was to explore the effects of CHR on HS and its underlying mechanisms. TGF-β1-induced HDF-α (Human Dermal Fibroblasts) served as an in vitro model of HS. Following treatment with CHR, cellular viability, proliferation, migration, and contractile capacity were evaluated through CCK-8, EdU, Transwell, wound healing, and collagen gel contraction assays. Western blot analysis was conducted to evaluate the expression levels of PCNA, MMP-2, α-SMA, Collagen I, and Collagen III, along with the activation status of the TGF-β/Smad signaling pathway. In vivo, histological analysis of rabbit ear HS tissues demonstrated that CHR ameliorated fibroblast proliferation and improved collagen fiber organization. Furthermore, immunohistochemical and Western blot analyses showed that CHR downregulated the expression levels of α-SMA, Collagen I, and Collagen III. Therefore, CHR may be a potential drug for the prevention and treatment of HS.</p>\u0000 </div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144998559","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":"TRIB1 silencing attenuates epilepsy by restoring mitochondrial homeostasis and suppressing microglia-driven neuroinflammation via MAPK pathway inhibition","authors":"Chunying Liao,&nbsp;Jie Cao,&nbsp;Hanyi Zeng,&nbsp;Cuiyin Chen,&nbsp;Jianqing Yuan","doi":"10.1007/s10735-025-10580-7","DOIUrl":"10.1007/s10735-025-10580-7","url":null,"abstract":"<div>\u0000 \u0000 <p>We aim to explore the role of Tribbles homolog 1 (TRIB1) in epilepsy (EP), specifically its modulation of mitochondrial homeostasis and the mitogen-activated protein kinase (MAPK) pathway. Gene expression profiling, differentially expressed genes screening, functional enrichment analysis, and protein-protein interaction (PPI) network construction were conducted to identify hub genes. Lipopolysaccharide (LPS)-induced BV2 cell models and lithium-pilocarpine-induced EP rat models were established to explore the impact of TRIB1 knockdown on EP development. The severity of EP in rats was evaluated by Racine scale, hematoxylin-eosin staining, and Nissl staining. Cell dysfunction was assessed by detecting cell viability, apoptosis, and oxidative stress markers. Western blot was applied to detect proteins related to mitochondrial function, microglial activation, and the MAPK pathway. We identified 16 hub genes from PPI networks. Among them, TRIB1 was upregulated in EP rats. In EP rat models, TRIB1 knockdown reduced seizure severity, improved oxidative stress, and enhanced mitochondrial homeostasis. TRIB1 knockdown increased viability, inhibited apoptosis, and restored mitochondrial homeostasis in LPS-induced BV2 cells. Moreover, TRIB1 knockdown attenuated microglia activation and neuroinflammation both in vivo and in vitro. TRIB1 knockdown suppressed the MAPK pathway in LPS-induced BV2 cells. The activation of the MAPK pathway reversed the alleviating effect of TRIB1 silencing on LPS-induced BV2 cell and mitochondrial function, as well as microglia-induced neuroinflammation. Knockdown of TRIB1 may provide novel therapeutic strategies for managing EP by restoring mitochondrial homeostasis and inhibiting neuroinflammation driven by microglial activation via the MAPK pathway.</p>\u0000 </div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144990391","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":"Changes in galectin-1 expression in pulp tissue and CD68 + macrophages in irreversible pulpitis and healthy pulp","authors":"José Antonio Mestas-Ramos,&nbsp;María Cristina Franco-Arellanes,&nbsp;Luis Enrique Ambrosio-Castillo,&nbsp;Ulises González-González,&nbsp;María Elena Hernández-Aguilar,&nbsp;Saira Karina Ramírez-Thomé,&nbsp;Jesús Hernández-Juárez,&nbsp;Beatriz Xóchitl Ávila-Curiel,&nbsp;Edgar Zenteno,&nbsp;Carlos Josué Solórzano-Mata","doi":"10.1007/s10735-025-10583-4","DOIUrl":"10.1007/s10735-025-10583-4","url":null,"abstract":"<div><p>Galectin-1 is a protein from the lectin family that is capable of recognizing β-galactosides, and it is involved in modulating the inflammatory response and tissue homeostasis. However, the presence and distribution of galectin-1 in pulp tissue, as well as its role in pulp inflammation, are poorly understood. Although galectin-1 has been reported to be present in healthy and necrotic pulp tissue at the proteomic level, the modifications and implications of these changes in galectin in tissues with irreversible pulpitis and infiltrating macrophages that could help clarify the inflammatory phenomenon have not yet been described. Objective: To determine the presence and distribution of galectin-1 in the dental pulp and in macrophages in tissues with irreversible pulpitis and healthy pulp. Materials and Methods: Immunofluorescence assays were performed on tissues from patients with irreversible pulpitis and their healthy counterparts to explore the presence of galectin-1 in different pulp regions. In addition, galectin-1 was detected in tissue macrophages (CD68 +). Images were analyzed via Fiji/ImageJ software. Results: Our data revealed that galectin-1 is expressed in both healthy pulp tissue and tissue with irreversible pulpitis, with a greater intensity of galectin-1 in tissues with irreversible pulpitis. Odontoblasts and macrophages (CD68 +) colocalized with galectin-1. Our findings indicate a higher number of CD68 + macrophages in the peripheral region of healthy pulp tissue, and that Gal-1 is expressed in these cells under both inflammatory and non-inflammatory conditions. Conclusion: Galectin-1 is present in tissues from patients with irreversible pulpitis and their healthy counterparts. Gal-1 is a molecule anti-inflammatory, suppressive, and pro-resolving functions, Gal-1 could potentially mitigate the pulpal inflammatory response and influence macrophage M2 polarization with the aim of preserving pulp vitality. Elucidating the precise function of galectin-1 in dental pulp will be a crucial focus of future research.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144990392","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":"FAM49B mediates tumor progression and poor prognosis of gastric cancer through activating PI3K/AKT pathway","authors":"Huimin Yang,&nbsp;Yanxia Ji,&nbsp;Yingzhe Ju,&nbsp;Yingying Shen,&nbsp;Xiaoyi Sun,&nbsp;Kaili Dai","doi":"10.1007/s10735-025-10589-y","DOIUrl":"10.1007/s10735-025-10589-y","url":null,"abstract":"<p>Gastric cancer is a common malignancy worldwide. It has been shown that the actin cytoskeleton modulator family with sequence similarity 49 member B (FAM49B) is involved in the initiation and spread of malignancies. However, the role of FAM49B is still unknown in gastric cancer. We examined FAM49B expression in gastric cancer and its relationship between the clinical pathological features of gastric cancer patients. Lentiviruses packaged sh-FAM49B were transfected into AGS cells, and the FAM49B overexpression plasmids were transfected into HGC-27 cells to perform loss- or gain-of-function assays. Additionally, AGS cells expressing sh-FAM49B were subcutaneously injected into nude mice. In vitro and in vivo experiments were conducted to investigate the role and mechanism of FAM49B in the progresses of gastric cancer. FAM49B was upregulated in gastric cancer that indicated a poor prognosis of gastric cancer patients. FAM49B enhanced cell viability, the percent of EdU positive cells, invaded cell numbers, the relative protein expression level of PD-L1 and the IL-10 concentration, while reduced the percent of CD8 + T cells and the concentration of IFN-γ in vitro. In tumor-bearing mice, knockdown of FAM49B reduced tumor size and weight, and the protein levels of PD-L1 and IFN-γ. FAM49B promoted the expressions of the PI3K/AKT/mTOR axis in vitro and in vivo. Inhibitory role of the FAM49B knockdown in the above-mentioned progresses was reversed with the treatment of 740Y-P. Therefore, FAM49B promoted the gastric cancer cell growth, invasion and immune escape through the PI3K/AKT/mTOR axis.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144929304","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":"Effects of depression on thyroid function, pathology and ultrasonography in rats","authors":"Xueyan Wu,&nbsp;Yingjing Gao,&nbsp;Siyan Liu,&nbsp;Lei Meng,&nbsp;Shaolian Wang,&nbsp;Chunhong Song","doi":"10.1007/s10735-025-10584-3","DOIUrl":"10.1007/s10735-025-10584-3","url":null,"abstract":"<div>\u0000 \u0000 <p>To investigate the effects of depression on thyroid function, pathology, and ultrasonography in rats, focusing on inflammatory markers and therapeutic interventions. Depression model rats were randomly divided into three groups: model group, fluoxetine group, and Jingqianshu granules group (10 g/kg/day)—a traditional Chinese medicine with antidepressant and anti-inflammatory effects. Depression was induced through chronic restraint stress. Thyroid function was assessed using serum T3, T4, FT3, FT4, and TSH via ELISA. Immunohistochemistry measured IL-1β, IL-2, IL-4, IL-6, IL-10, TNF-α, and IFN-γ in thyroid tissue. HE staining evaluated histological changes, and ultrasound assessed thyroid echogenicity. The model group showed increased expression of IL-1β, IL-2, IL-6, and TNF-α, and decreased IL-10 and IFN-γ (<i>p</i> &lt; <i>0.05</i>). Fluoxetine significantly reduced IL-6 (<i>p</i> &lt; <i>0.05</i>), while Jingqianshu granules notably decreased TNF-α and IL-1β levels (<i>p</i> &lt; <i>0.05</i>). Thyroid epithelial cells in the model group showed damage, atrophy, and reduced colloid content. Treatment groups showed partial improvement and reduced lymphocyte infiltration. Compared to controls, thyroid echo was significantly diminished in the model group (<i>p</i> &lt; <i>0.01</i>); treatment groups improved. The model group exhibited elevated FT3 and FT4 levels and reduced TSH, indicating thyroid dysfunction. Both treatment groups showed partial normalization of these hormone levels. Both fluoxetine and Jingqianshu granules alleviated depression-induced thyroid pathological and imaging changes, with Jingqianshu demonstrating partial anti-inflammatory effects and potential as a complementary treatment. Further studies are needed to confirm their efficacy and safety relative to fluoxetine. These findings support further study into depression-related thyroid dysfunction.</p>\u0000 </div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144929308","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":"Atorvastatin improves long-term memory by reducing amyloid-β formation and neuronal damage in STZ-induced diabetic rats","authors":"N. Ferak,&nbsp;A. Kapucu,&nbsp;S. Ustunova,&nbsp;K. Akgun-Dar","doi":"10.1007/s10735-025-10564-7","DOIUrl":"10.1007/s10735-025-10564-7","url":null,"abstract":"<div>\u0000 \u0000 <p>Diabetes mellitus is associated with decline in cognitive function and changes in brain structure. Statins have received increasing attention to be used as neuroprotective drug. We examined the neuroprotective effects of atorvastatin on neuropathological alterations such as learning and memory performance, the amyloid-β formation, and expression of nitric oxide synthases (NOSs) in hippocampus of streptozotocin (STZ)-induced diabetic rats. Adult male Wistar rats were divided into four groups; The normal control group, STZ-induced diabetes group, STZ-induced diabetic rats followed by treatment with atorvastatin group and normal rats treated with atorvastatin. The passive avoidance test was used to evaluate the learning and memory status of animals. Blood and hippocampus samples were obtained for biochemical and histological analysis. The expressions of nitric oxide synthases were immunohistochemically detected, and histopathological changes of amyloid beta were examined using Congo red stain in CA1 region of hippocampus. Count of congo red positive cells in CA1 region increased in diabetic rats, however atorvastatin treatment decreased it. Amyloid-β levels and S100B levels in the hippocampus and plasma increased in diabetic rats, atorvastatin treatment decreased. Total nitrite-nitrate levels increased, while iNOS expression decreased in the CA1 area of hippocampus in atorvastatin treated diabetic rats, eNOS and nNOS expression increased. The retention latency times of diabetes group decreased, however atorvastatin treatment to diabetic rats prolonged at the 48th hour and 72nd hour. Atorvastatin improved the long-term memory by suppressing the formation of amyloid-β, increasing eNOS and nNOS protecting the blood brain barrier in diabetic rats.</p>\u0000 </div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144929306","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":"HIF-1α-mediated inhibition of the sFlt-1/sENG/TNF-α pathway promotes angiogenesis to ameliorate pre-eclampsia","authors":"Jie Liu,&nbsp;Mengmeng Zhao,&nbsp;Suqin Zhang,&nbsp;Yanmei Shi","doi":"10.1007/s10735-025-10579-0","DOIUrl":"10.1007/s10735-025-10579-0","url":null,"abstract":"<div><p>Pre-eclampsia (PE) is a common pregnancy complication, closely associated with endothelial dysfunction and inhibition of angiogenesis. This study aims to explore the pathological mechanisms causing endothelial dysfunction and suppressed angiogenesis in PE, with the aim of identifying potential drug targets. Human umbilical vein endothelial cells (HUVECs) were exposed to angiotensin II (Ang-II) to mimic PE-related endothelial dysfunction. Angiogenic capacity was evaluated using tube formation assay, scratch assay, flow cytometry, and CCK-8 assay. A Reduced Uterine Perfusion Pressure (RUPP) mouse model was established to recapitulate PE. Expression profiles of hypoxia-inducible factor-1α (HIF-1α), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), vascular endothelial growth factor (VEGF), placental growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin (sENG), and tumor necrosis factor-α (TNF-α) were quantified via Western blot and RT-qPCR. Biochemical assessments included levels of malondialdehyde, superoxide dismutase, glutathione, and the urine protein/creatinine (UP/cr) ratio. Systolic blood pressure was measured while placental histopathology was examined using hematoxylin and eosin (HE) staining. In HUVECs exhibiting endothelial dysfunction, ICAM-1 and VCAM-1 were markedly upregulated, whereas HIF-1α expression was significantly reduced. Overexpression of HIF-1α boosted HUVEC proliferation and migration, attenuated apoptosis and oxidative stress, enhanced expression of VEGF and PlGF, and suppressed expression of sFlt-1, sENG, and TNF-α, thereby promoting angiogenesis. In the RUPP-modeled PE mouse model, diminished HIF-1α expression coincided with elevated ICAM-1 and VCAM-1, leading to endothelial dysfunction, elevated systolic blood pressure, and increased UP/cr ratio. Conversely, HIF-1α overexpression ameliorated placental tissue damage and oxidative stress, upregulated VEGF and PlGF, downregulated sFlt-1, sENG, TNF-α, ICAM-1, and VCAM-1, and restored angiogenic capacity. HIF-1α ameliorates endothelial dysfunction in PE by suppressing the sFlt-1/sENG/TNF-α signaling pathway, thereby promoting angiogenesis and alleviating PE.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144929305","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":"Huangqi Guizhi Wuwu Decoction inhibits ferroptosis to improve cyclophosphamide induced immunosuppression through regulation of arachidonic acid metabolism","authors":"Li Wang,&nbsp;Fenyun Liu,&nbsp;Qianqian Wan,&nbsp;Yafei Xia,&nbsp;Qi Zhang,&nbsp;Jing Xun,&nbsp;Ping Li,&nbsp;Yuming Wang,&nbsp;Mei Li,&nbsp;Yuhong Bian,&nbsp;Huantian Cui","doi":"10.1007/s10735-025-10582-5","DOIUrl":"10.1007/s10735-025-10582-5","url":null,"abstract":"<div>\u0000 \u0000 <p>Huangqi Guizhi Wuwu Decoction (HGWD) has shown laboratory efficacy in autoimmune diseases, however its effectiveness and mechanism in addressing the decline of immune function remain unclear. We first established a cyclophosphamide-induced mouse model of immunosuppression and evaluated various immune indicators to determine the efficacy of HGWD in improving the immune function of CTX-immunosuppressed mice. Next, we conducted serum non-targeted metabolomics analysis to investigate HGWD’s effects on serum differential metabolites and used KEGG pathway enrichment analysis to identify the key pathways through which HGWD improves immune function. Finally, we validated HGWD’s impact on arachidonic acid (AA) metabolism and ferroptosis. HGWD treatment significantly improves the number of immune cells, ameliorates thymus and spleen tissue pathology, and restores the immune function. Non-targeted metabolomics analysis indicated that AA metabolism was a common pathway among the control group, CTX group, and H-HGWD group. HGWD intervention resulted in downregulation of serum levels of 15(S)-HpETE, 16(R)-HETE, Prostaglandin H2, and Prostaglandin G2 in CTX-immunosuppressed mice, while upregulating the level of 12(S)-HETE. RT-qPCR and Western blot analyses revealed that HGWD intervention significantly downregulated the expressions of ALOX15, CYP2C, ALOX12, and COX1, while upregulating GPX4 expression. Furthermore, HGWD intervention reduced TUNEL-positive expression in spleen tissue, improved levels of ferroptosis-related factors (total iron, MDA, 4-HNE, GSH/GSSG), and modulated expressions of ferroptosis-related proteins (FTL, FTH, TRF, and ACSL4). Our research has confirmed the significant potential of HGWD in improving the immune function of CTX-immunosuppressed mice. Specifically, HGWD may improve immune function by regulating AA metabolism to inhibit ferroptosis.</p>\u0000 </div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144929307","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":"Prenatal and pubertal exposure to ethinylestradiol induces Long-Term stromal and epithelial changes in the gerbil dorsal prostate","authors":"Thaiz Furtado Silva,&nbsp;Bárbara Gomes,&nbsp;Camila Souza Crosgnac,&nbsp;Bruno Vinícius Aguiar,&nbsp;Pedro Augusto Barbosa Silva,&nbsp;Sebastião Roberto Taboga,&nbsp;Ana Paula da Silva Perez","doi":"10.1007/s10735-025-10568-3","DOIUrl":"10.1007/s10735-025-10568-3","url":null,"abstract":"<div>\u0000 \u0000 <p>17α-Ethinylestradiol (EE2) is a synthetic estrogen derived from 17β-estradiol and widely used in oral contraceptives. It interferes with the endocrine system and disrupts hormonal balance. This study investigated the long-term effects of prenatal and pubertal EE2 exposure on the dorsal prostate of aging gerbils. Adult female gerbils (90–120 days old) received EE2 (15 µg/kg/day) and were assigned to three groups (n = 5): Control (untreated), EE2/PRE (exposed during gestational days 18–22), and EE2/PUB (exposed during postnatal days 42–49). After 12 months, the animals were euthanized, and dorsal prostates were collected for biometric, histopathological (including quantification of prostatic acini/section and lesion multiplicity), and Morphometric analyses (epithelial height and muscle thickness), with stereological evaluation of the epithelium, lumen, muscle, stroma, blood vessels, and collagen fibers. Tissue sections were stained with Hematoxylin–Eosin, Gömori’s Trichrome, and Picrosirius Red. Results showed increased muscular thickness and decreased vascular volume in the EE2/PRE group, while the EE2/PUB group exhibited reduced volumes of the epithelium, lumen, and collagen fibers. Lesion analysis revealed a reduction in prostatic intraepithelial neoplasia (PIN) and an increase in luminal inflammation in the EE2/PUB group. These findings indicate that the biological effects of EE2 vary according to the timing of exposure, with both prenatal and pubertal periods representing critical developmental windows. EE2 exposure during these stages can induce alterations in epithelial-stromal interactions in a lobe-specific manner. Hormonal imbalance triggered ERα/ERβ signaling, influencing cellular differentiation and promoting inflammation. These distinct outcomes highlight how endocrine-disrupting chemicals (EDCs) compromise prostate homeostasis through hormone reprogramming and receptor-mediated pathways.</p>\u0000 </div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144914640","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}