European Journal of Histochemistry最新文献

{"title":"Electroacupuncture combined with rTMS promotes neuronal regeneration <i>via</i> DNMT1-mediated PI3K-AKT pathway in cerebral palsy model.","authors":"Juan Fan, Yu Ma, Liying Sun, Suhua Miao, Jianghong He","doi":"10.4081/ejh.2026.4533","DOIUrl":"10.4081/ejh.2026.4533","url":null,"abstract":"<p><p>Cerebral palsy (CP), resulting from perinatal brain injury, is characterized by persistent motor dysfunction largely due to impaired regeneration of the corticospinal tract. Electroacupuncture (EA) and repetitive transcranial magnetic stimulation (rTMS) are promising non-invasive neuromodulation approaches, but their combined effects and epigenetic mechanisms remain unclear. This study examined the synergistic neurorestorative potential of EA and rTMS in a hypoxic-ischemic brain damage (HIBD) model of CP, focusing on DNA methyltransferase 1 (DNMT1) regulation of the PI3K-AKT pathway. In vivo, neonatal rats subjected to HIBD were assigned to control, HIBD, EA, rTMS, or combined EA+rTMS groups and treated for four weeks. Motor function was assessed using rotarod, grid-walking, and grip strength tests, while neuronal and molecular changes were analyzed via histological and biochemical methods. In vitro, hypoxia-exposed cortical neurons underwent DNMT1 and PI3K modulation to clarify mechanisms. Combined EA+rTMS produced superior functional recovery compared to monotherapies, including a 2.1-fold increase in rotarod latency, 53% reduction in foot faults, and 80% improvement in grip strength vs untreated HIBD animals. Improvements were also greater than EA or rTMS alone. Histological findings showed enhanced neuronal density in cortical and spinal regions. At the molecular level, combined treatment suppressed DNMT1 expression and increased PI3K, phosphorylated AKT, GAP-43, and myelin basic protein. In vitro, DNMT1 knockdown enhanced PI3K-AKT signaling, neuronal survival, and axonal growth, while DNMT1 overexpression or PI3K inhibition negated these effects. Overall, EA+rTMS promotes functional and structural recovery in CP by epigenetically inhibiting DNMT1 and activating the PI3K-AKT pathway, supporting its translational potential for perinatal brain injury.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13122296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147724589","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":"Ketogenic diet regulates Uch-L1(C) to improve cerebral energy metabolism and cognitive function in Alzheimer's disease mice.","authors":"Nana Bao, Min Zhang, Ming Tang, Ziyi Shen, Shenglin Wang, Guohui Jiang","doi":"10.4081/ejh.2026.4548","DOIUrl":"10.4081/ejh.2026.4548","url":null,"abstract":"<p><p>The ketogenic diet (KD), a high-fat, low-carbohydrate diet, can effectively regulate energy metabolism in the brain. The regulation of cerebral energy metabolism in patients with Alzheimer's disease (AD) has attracted the attention of researchers. Recent studies have shown that ubiquitin carboxyl terminal hydrolase L1 (Uch-L1) deficiency leads to neurodegeneration by increasing energy demand and endoplasmic reticulum stress. However, the effect of Uch-L1 on AD remains to be explored. This study first combined Uch-L1 with cerebral energy metabolism to explore its role in long-term KD in AD. We found that AD mice with long-term KD showed better spatial recognition and working memory. KD promoted Uch-L1(C) and Mfn2 expression by inhibiting oxidative stress in the hippocampus of mice, improved mitochondrial function, increased ATP content, and significantly reduced neuronal apoptosis. In conclusion, KD can increase Uch-L1(C) and Mfn2 expression in the brain, and improve cerebral energy metabolism and cognitive function in AD mice.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13122298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147724653","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":"Senolytics alleviate cyclophosphamide-induced premature ovarian insufficiency by eliminating senescent cells.","authors":"Huina Su, Ruiqiong Ma, Dehui Su, Cheng Tan, Ye Zhu, Xin Yang","doi":"10.4081/ejh.2026.4537","DOIUrl":"10.4081/ejh.2026.4537","url":null,"abstract":"<p><p>Alkylating agents, particularly cyclophosphamide (CY), are known for their high toxicity, which can lead to iatrogenic premature ovarian insufficiency (POI) and infertility in young cancer survivors. Currently, effective prevention and treatment strategies remain limited. Given that chemotherapy induces cellular senescence, we investigated the therapeutic potential of dasatinib (D) and quercetin (Q), a senolytic combination known to eliminate senescent cells. Using a CY-induced murine model of ovarian injury, we found that CY treatment increased the accumulation of senescent cells in the ovaries. The resulting senescence-associated secretory phenotype (SASP) led to a deterioration of the ovarian microenvironment, characterized by increased follicular atresia and a decline in follicle quantity, ultimately culminating in POI. Our findings demonstrate that DQ therapy effectively mitigated CY-induced damage by clearing senescent cells and reducing SASP secretion. Clinically, DQ administration restored sex hormone levels and regularity of the estrous cycle, resulting in an overall increase in follicle numbers across all developmental stages. Furthermore, DQ treatment significantly normalized estrous cyclicity, restoring regular cycles in 60% of the CY+DQ mice compared to only ~15% in the CY-alone group (p<0.0001). RNA sequencing analysis revealed that DQ treatment upregulated Pagr1a, a gene associated with extraembryonic development, while downregulating genes involved in senescence induction (Itgb3, Wnt10b, Vegfa) and immune function (A2m, Ccl21d). These results suggest that senescent cells drive CY-induced ovarian damage and that DQ represents a promising therapeutic strategy for preserving the ovarian reserve and endocrine function in female cancer patients.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147730569","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":"Immunohistochemical detection of putative pathogenetic factors in adhesions of infants: a pilot study.","authors":"Arvis Pauliņš, Anna Junga, Māra Pilmane","doi":"10.4081/ejh.2026.4438","DOIUrl":"10.4081/ejh.2026.4438","url":null,"abstract":"<p><p>Newborns' intestinal adhesions have been reported in 4.7% infants who underwent a laparotomy, but adhesions can also appear idiopathically. Etiology and pathogenesis of adhesions is still to be determined, but evidence shows relation to inflammation, formation of fibrin bands, hypoxia and tissue remodelation. Multiple candidate genes have been associated with adhesion development. The aim of this study was to evaluate the appearance of Sonic Hedgehog (SHH), Indian Hedgehog (IHH), Forkhead-box F1 (FOXF1), caudal type homeobox 1 (CDX1), HCLS1-associated protein X-1 (HAX-1), GATA Binding Protein 4 (GATA4) and Granzyme-B (GZMB) proteins in infant adhesions and to describe possible interfactorial correlations. Adhesion affected tissue samples were collected from 14 patients under one year of age that underwent abdominal surgery to treat partial or complete intestinal obstruction. The control group consisted of 6 individuals that had surgical repairment of inguinal hernia. Routine staining and immunohistochemistry were performed. Immunopositive fibroblasts, macrophages, endotheliocytes, smooth muscle myocytes of blood vessel wall and mesotheliocytes were investigated. The relative distribution of all factors was evaluated by the semiquantitative counting method. Statistical analysis was done using non-parametric tests and correlations were calculated based on Spearman's correlation analysis. A statistically significant decrease was observed for SHH, IHH, FOXF1, GATA4 and partially for GZMB in the adhesion group. There were also decreased HAX-1 and CDX1 immunopositive structures in the adhesion group, however, without any statistical significance. SHH, IHH, FOXF1, GATA4 and GZMB might have a role in adhesion development among infant patients which could suggest a dysregulation of cellular events. Abundance of correlations between the gene protein appearances in different structures indicate the affected blood vessels, fibroblasts and macrophages, however, mesothelium seems not to be the key driver in the morphopathogenesis of adhesion development.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12947813/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146182620","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":"Back to the future: improving storage of Golgi-stained mouse brain.","authors":"Fabrizio De Luca","doi":"10.4081/ejh.2026.4532","DOIUrl":"10.4081/ejh.2026.4532","url":null,"abstract":"<p><p>Morphological analysis of neuronal processes and their networks is a key aspect of neuroscience, with relevance from basic research to clinical practice due to the central role of neuronal development and plasticity in many neurological disorders. More than a century after its introduction, Golgi staining, a technique based on the random precipitation of metallic deposits in different neuronal subtypes, remains a highly valuable method for investigating the cellular morphology of neurons in the nervous system. Despite the wide range of protocols developed over the years, several limitations of the technique remain a matter of discussion. Among these is the need to extend sample preservation during the interval between staining and sectioning procedures without compromising the quality of the histochemical labeling. By adopting a specific processing method, the present study demonstrates that it is possible to embed murine nervous tissue following Golgi staining and to preserve the samples for extended periods prior to sectioning, while maintaining well-preserved and clearly detectable histochemical labeling across different regions and neurons of the mouse central nervous system.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13003391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147357595","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":"SRSF3 promotes the generation of XBP1s to stabilize autophagy and enhance hypoxia adaptation in glioma.","authors":"Bohu Liu, Xiaoran Zhang, Jintao Tian, Xiaobin Huang, Xuhui Li, Jinxi Zhao, Zhenghu Xu, Jun Pu","doi":"10.4081/ejh.2026.4530","DOIUrl":"10.4081/ejh.2026.4530","url":null,"abstract":"<p><p>Hypoxia is a key driver of glioblastoma (GBM) progression. Serine/arginine-rich splicing factor 3 (SRSF3) is associated with the malignant progression of GBM, but its role in the hypoxic microenvironment of GBM remains unclear. This study aimed to explore the regulatory role and molecular mechanisms of SRSF3 in hypoxia adaptation in GBM. The expression of SRSF3 in normal astrocytes and GBM cells was detected. The effects of knockdown or overexpression of SRSF3 combined with hypoxia treatment on malignant phenotypes and hypoxia stress adaptation in GBM cells were evaluated. Cell viability, colony formation, migration, invasion, and cell death assays were performed to assess phenotypic changes. Mechanisms were investigated using mRFP-GFP-LC3, autophagy, and unfolded protein response (UPR)-related molecular detection. SRSF3 was highly expressed in GBM cells. Knockdown of SRSF3 inhibited cell viability, migration, invasion, and colony formation, whereas overexpression of SRSF3 promoted malignant behaviors. Further studies revealed that hypoxia induction significantly increased the expression levels of GRP78, CHOP, ATF4, LC3-II/I, and p62; upregulated the GFP/mRFP ratio; and increased cleaved-caspase3 expression, promoting cell death. Mechanistic studies revealed that SRSF3 overexpression promoted XBP1s formation, alleviated hypoxia-induced autophagic flux blockage, and reduced cell death. The IRE1 RNase inhibitor 4μ8C weakened the SRSF3-mediated promotion of XBP1s generation. SRSF3 enhances adaptive UPR output by promoting IRE1-dependent XBP1 splicing, thereby maintaining autophagic flux and promoting GBM cell survival under hypoxic conditions.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13003393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147357512","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":"Overexpression of GPER1 suppressed esophageal carcinoma growth <i>via</i> activating cAMP pathway.","authors":"Hongmei Yin, Xiumei Han, Qun Zhang, Duojie Li, Fan Wang","doi":"10.4081/ejh.2026.4422","DOIUrl":"10.4081/ejh.2026.4422","url":null,"abstract":"<p><p>G protein-coupled estrogen receptor 1 (GPER1) has extensively verified as a tumor regulator in various types of cancers. However, its role in esophageal cancer (EC) remains largely unclear. In this study, the expression and prognostic prediction value of GPER1 in EC was analyzed by using TCGA database and was verified in EC cells and fresh tissues. The results showed that GPER1 is decreased in EC cells and tissues, and lower GPER1 expression is associated with poor overall survival of EC patients. CCK-8 assay and flow apoptosis cytometry were applied to measure the ability of proliferation and apoptosis of EC cells with or without GPER1 overexpression. The levels of reactive oxygen species (ROS) and Fe2+ were determined by flow cytometry. Elisa and Western blotting were employed to measure the markers of ferroptosis and cyclic adenosine monophosphate (cAMP) pathway. The results of in vitro experiments indicated that overexpression of GPER1 caused decreased proliferation, increased cell apoptosis, ROS generation, Fe2+ content and acyl-CoA synthetase long-chain family member 4 (ACSL4) expression, while decreased glutathione peroxidase 4 (GPX4) expression. Notably, the cAMP/PKA inhibitor H89 significantly reversed the ferroptotic effects induced by GPER1, indicating the essential role of the cAMP pathway in this process. The weight and volumes of tumors were measured and Ki-67 and H&E staining were conducted to analyze the effect of GPER1 in vivo. The results of in vivo experiments indicated that overexpression of GPER1 resulted in restricted tumor growth, reduced Ki-67 expression and increased cell death. In conclusion, the expression of GPER1 is reduced in EC. Overexpression of GPER1 enhances ferroptosis in EC, primarily through activation of the cAMP signaling pathway.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12878560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146054696","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":"Low ozone concentrations promote <i>in vitro</i> preservation of explanted articular cartilage: an ultrastructural study.","authors":"Giada Remoli, Chiara Rita Inguscio, Federico Boschi, Gabriele Tabaracci, Manuela Malatesta, Barbara Cisterna","doi":"10.4081/ejh.2026.4440","DOIUrl":"10.4081/ejh.2026.4440","url":null,"abstract":"<p><p>Ozone (O3) is an oxidizing natural gas widely applied as adjunctive therapeutic treatment for a variety of pathological conditions. Currently, O3-based therapies rely on the low-dose concept i.e., the administration of low O3 concentrations able to induce a mild oxidative stress stimulating antioxidant and anti-inflammatory response without causing cell damage. In addition, low O3 concentrations are thought to activate cellular and molecular mechanisms responsible for analgesic and regenerative effects. Due to these properties, in the last decade interest has arisen in the fields of orthopedics and regenerative medicine on the potential of O3 to counteract joint diseases involving cartilage degeneration. In this pilot study, we have explored the anti-degenerative potential of O3 on knee articular cartilage explanted from a healthy adult rabbit and maintained in vitro. Light and transmission electron microscopy were used to monitor chondrocyte and extracellular matrix features of cartilage samples undergoing O3 treatment every three days for two weeks. Results demonstrated that low O3 concentrations act on chondrocytes and the molecular components of the extracellular matrix of articular cartilage explants, significantly improving their preservation under in vitro conditions, likely by promoting both protective and pro-regenerative pathways. This opens promising perspectives for further investigations on the therapeutic potential of O3 for the treatment of cartilage degeneration not only as painkilling and anti-inflammatory agent but also as a cartilage regenerative agent.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12878561/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146054623","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":"Histopathological and immunofluorescent characterization of post-sepsis immune dysregulation in a clinically relevant mouse model.","authors":"Haoran Tang, Chen Liao, Ning Tang, Hui Li, Yi Liu, Lingling Wang, Zongfang Ren","doi":"10.4081/ejh.2026.4435","DOIUrl":"10.4081/ejh.2026.4435","url":null,"abstract":"<p><p>Sepsis remains a major cause of morbidity and mortality worldwide, yet its prolonged pathophysiological consequences are poorly understood. Here, we employed a murine cecal ligation and puncture (CLP) model to investigate the prolonged impact of sepsis on survival, systemic inflammation, and organ pathology. Adult male C57BL/6 mice underwent CLP or sham surgery and were monitored for 28 days. Survival was recorded daily, while serial assessments of hematology, serum biochemistry, bacterial load, and cytokine levels were performed. Tissue immunofluorescence was used to characterize myeloid-derived suppressor cells (MDSCs), which are potent immunosuppressive cells that inhibit both adaptive and innate immune responses in sepsis, contributing to sepsis-induced immunosuppression. Histopathological analyses were conducted to evaluate structural changes in major organs. CLP mice displayed markedly reduced long-term survival compared with sham controls. Hematological profiling revealed persistent leukocytosis and an inflammatory response, while serum analyses showed sustained elevations in in bilirubin, creatinine, and blood urea nitrogen, reflecting hepatic and renal injury. Bacterial cultures confirmed systemic microbial persistence, and cytokine measurements indicated ongoing inflammatory activity. Tissue immunofluorescence demonstrated the infiltration of MDSCs across multiple organs, consistent with post-sepsis immunosuppression. Histopathological examination revealed widespread, chronic injury in the lungs, liver, kidneys, and spleen, including inflammatory infiltration, tissue degeneration, and architectural disruption. In conclusion, sepsis induces not only acute systemic inflammation but also enduring immune dysregulation and progressive organ damage. These findings highlight the CLP model as a robust platform for studying post-sepsis sequelae and underscore the need for therapeutic strategies that target long-term organ protection and immune restoration.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12947808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146183235","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":"Cryptotanshinone alleviates DSS-induced colitis in mouse by regulating the balance of Treg/Th17 cells and M1 macrophage activation.","authors":"Lin Liu, Wei Huang, Yu Wu, Guanlong Ye, Jing Zhang, Tong Shen, Changjuan Ouyang","doi":"10.4081/ejh.2026.4436","DOIUrl":"10.4081/ejh.2026.4436","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD) including ulcerative colitis (UC) and Crohn's disease has become a global disease in the 21st century, with increasing incidence rates in almost every industrialized country. Previous studies have suggested that the traditional Chinese medicine herb, cryptotanshinone (CTN), a major liposoluble extract of Salvia miltiorrhiza, alleviates the symptoms of experimental colitis in vitro and in vivo. However, the mechanisms underlying the protective effects of CTN against IBD remain exclusive. The present study found that CTN reversed lipopolysaccharide-induced inflammation in human colon epithelial cells (HIEC-6) by inhibiting the NF-κB pathway. In addition, CTN alleviated dextran sulfate sodium (DSS)-induced inflammatory bowel disease in mice by regulating the balance of TH17/Treg cells. CTN also exerted its role by inhibiting the polarization of M1 macrophages in mice with DSS-induced colitis. Of note, the effects of CTN on these immune cells may be mediated via changes in the levels of TNF-α and IL-6 directly in mice. Taken together, these findings may provide new insight regarding the therapeutic potential of CTN for UC.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12968986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146229829","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}