Journal of Molecular Histology最新文献

{"title":"Repurposing disulfiram: targeting Zeb1 to attenuate paraquat-induced pulmonary fibrosis in rats","authors":"Fatemeh Karimzadeh,&nbsp;Abdolreza Daraei,&nbsp;Ebrahim Zabihi-Neyshaburi,&nbsp;Farideh Feizi,&nbsp;Mohammad Ranaee,&nbsp;Soraya Khafri,&nbsp;Zohre Esmaeili,&nbsp;Zahra Babazadeh","doi":"10.1007/s10735-025-10613-1","DOIUrl":"10.1007/s10735-025-10613-1","url":null,"abstract":"<p>Pulmonary fibrosis is a fatal condition marked by excessive extracellular matrix deposition and myofibroblast activation, with paraquat (PQ) being a potent inducer via oxidative stress and profibrotic signaling. This study evaluated the antifibrotic effects of disulfiram (DSF), an FDA-approved medication, in rats with PQ-induced pulmonary fibrosis. Forty male Wistar rats were divided into eight groups receiving PQ (40 mg/kg) and DSF (1, 10, 100 mg/kg) for 21 days. Lung tissues were analyzed histopathologically (H&amp;E, Mallory’s trichrome) for inflammation, alveolar septal thickening, vascular congestion, and fibrosis, while <i>Zeb1</i> gene expression was assessed by real-time PCR. PQ exposure led to severe lung injury, collagen deposition, and significant upregulation of <i>Zeb1</i> (<i>p</i> = 0.0022). DSF at 10 mg/kg provided the most effective protection, significantly reducing histopathological damage and <i>Zeb1</i> expression (<i>p</i> &lt; 0.001). The 1 mg/kg dose showed moderate efficacy, and the 100 mg/kg dose had limited benefits, suggesting a dose-dependent toxicity. These findings indicate that DSF at 10 mg/kg attenuates PQ-induced pulmonary fibrosis by reducing inflammation, collagen accumulation, and <i>Zeb1</i>-mediated profibrotic signaling, supporting DSF as a potential repurposed antifibrotic therapy for PQ-induced and possibly idiopathic pulmonary fibrosis.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145073732","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":"Chinese ginger (Boesenbergia rotunda) mitigates diabetic nephropathy and cardiomyopathy by regulating oxidative inflammatory pathway","authors":"Chunhong Liu,&nbsp;Xiaolei Tang,&nbsp;Min Zhang,&nbsp;Yanhong Wu,&nbsp;Ademola Famurewa,&nbsp;Chitchamai Ovatlarnporn,&nbsp;Opeyemi Joshua Olatunji","doi":"10.1007/s10735-025-10559-4","DOIUrl":"10.1007/s10735-025-10559-4","url":null,"abstract":"<div><p>Chinese ginger (<i>Boesenbergia rotunda</i>) is a culinary and traditional medicinal plant in Southeast Asia and Indo-China regions with several medicinal benefits. This study aims to assess the effectiveness of Chinese ginger extract against diabetic nephropathy and cardiomyopathy and the associated signaling pathways. Animals were randomly assigned to groups; control rats, diabetic rats, diabetic rats treated with 100 and 400 mg/kg of the <i>B. rotunda</i> EtOAc fraction (BRE). Treatment was administered for 5 successive weeks via oral gavage. Thereafter, the rats were evaluated for fasting blood glucose, tumour necrosis factor alpha, interleukin-6, interleukin-1 beta, reduced glutathione, superoxide dismutase, catalase, lipid peroxidation activities. Gene expression levels of nuclear factor erythroid 2-related factor 2, and Kelch-like ECH-associated protein 1 were examined. Cardiorenal histopathological and immunohistochemical were performed to assess tissue damage. BRE administration to diabetic rats notably ameliorated changes in body weight, kidney and heart weight and fasting blood glucose level. Furthermore, in diabetic rats, BRE significantly reduced malonaldehyde, tumour necrosis factor alpha, interleukin-6, interleukin-1 beta levels considerably with increasing activity of antioxidant enzymes in the kidney and cardiac tissues of rats treated with BRE. Diabetic rats treated with BRE showed upregulated mRNA expression levels of nuclear factor erythroid 2-related factor 2, while Kelch-like ECH-associated protein 1 mRNA expression in the kidney and cardiac tissues were downregulated. In addition, BRE treatment significantly reduced the cardiorenal protein expression of Bcl2 and collagen IV in the immunohistochemical analyses. From the results of this study, it can be concluded that <i>B. rotunda</i> exerts cardiorenal protective effect on diabetic rats due to its antidiabetic and antioxidant and may be considered a treatment for T2DM.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145062301","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":"Protective effect of ambroxol on cyclophosphamide-induced intestinal damage: involvement of oxidative stress, inflammation, and Keap-1/Nrf2/HO-1 signaling","authors":"Reem S. Alruhaimi,&nbsp;Sulaiman M. Alnasser,&nbsp;Hanan S. Althagafy,&nbsp;Sherif M. A. Mansour,&nbsp;Omnia A. M. Abd El-Ghafar,&nbsp;Ayman M. Mahmoud,&nbsp;Emad H. M. Hassanein","doi":"10.1007/s10735-025-10599-w","DOIUrl":"10.1007/s10735-025-10599-w","url":null,"abstract":"<div><p>Cyclophosphamide (CP) is an effective chemotherapeutic agent whose clinical efficacy is often limited by toxicity, including intestinal injury. Oxidative stress and inflammation are central to CP-induced tissue damage and represent a valuable target to attenuate intestinal injury. Ambroxol (ABX), a clinically approved mucolytic agent, has demonstrated antioxidant, anti-inflammatory, and mucoregulatory properties that may confer multi-organ protection. This study investigated the protective effects of ABX against CP-induced intestinal injury in rats, exploring the involvement of oxidative stress, inflammation and Keap-1/Nrf2/HO-1 signaling. Adult male rats received ABX (20 mg/kg/day) orally for seven consecutive days, with CP (100 mg/kg, i.p.) administered on the fifth day. CP induced significant intestinal injury manifested by intestinal mucosal atrophy, decreased length of villi and goblet cell depletion. CP triggered oxidative stress characterized by increased MDA and decreased GSH, SOD, and catalase, upregulated NF-κB, IL-6, and TNF-α, and increased caspase-3 expression in the intestine. ABX attenuated histopathological alterations, mitigated oxidative stress, suppressed NF-κB and cytokines, and downregulated caspase-3. In addition, ABX preserved intestinal goblet cells while modulating the Keap-1/Nrf2/HO-1 pathway in intestinal tissue. These findings demonstrate the protective role of ABX against CP-induced intestinal injury via antioxidant, anti-inflammatory, and mucoprotective mechanisms, supporting its potential repurposing as an adjuvant during CP chemotherapy. The protective mechanism of ABX involves its ability to modulate the Keap-1/Nrf2/HO-1 signaling pathway.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145057716","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":"S1PR5 as a prognostic biomarker in colon cancer: insights into efferocytosis-related mechanisms and immune modulation","authors":"Aijie Pei,&nbsp;Ling Lu,&nbsp;Xiaolin Wu","doi":"10.1007/s10735-025-10608-y","DOIUrl":"10.1007/s10735-025-10608-y","url":null,"abstract":"<div><p>Colon cancer remains a major cause of global cancer mortality, characterized by complex interactions between genetic, epigenetic, and immune factors. This study investigates the prognostic value of efferocytosis-related genes and their role in colon cancer progression and immune modulation. A prognostic signature relied on efferocytosis-related genes was developed using univariate Cox and least absolute shrinkage and selection operator (LASSO) regression analyses. Immune infiltration, immune checkpoint expression, and tumor microenvironment characteristics were analyzed using single-sample gene set enrichment analysis (ssGSEA), ESTIMATE, and tumor immunophenotype (TIP) frameworks. S1PR5 was knocked down in SW1116 and SW620 cells. The effect of S1PR5 on colon cancer growth and macrophage regulation in vivo and in vitro. Colon cancer patients were stratified into high- and low-risk groups, with high-risk patients demonstrating significantly worse survival outcomes. S1PR5, a key gene in the model, was markedly overexpressed in colon cancer tumors and correlated with advanced clinical stages, poor survival outcomes, and diminished responses to immunotherapy. Furthermore, S1PR5 knockdown could inhibit colon cancer cell activity and increase macrophage polarization from M0 to M1. Our research developed an efferocytosis-related gene prognostic model and identified S1PR5 as a key biomarker. S1PR5 showed significant associations with advanced clinical stages, immunosuppressive microenvironments, and unfavorable survival outcomes, underscoring its potential as both a prognostic marker and a therapeutic target in colon cancer.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145057717","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":"MAO-A inhibition alleviates sepsis-driven lung injury via Nrf2/HO-1 pathway activation and suppression of pyroptosis","authors":"Min Li,&nbsp;Hu Li,&nbsp;Liming Gong,&nbsp;Xinmin Chen,&nbsp;Jincan Dai,&nbsp;Jirong Tian,&nbsp;Xiaochuan Yin,&nbsp;Qinghe Yu","doi":"10.1007/s10735-025-10560-x","DOIUrl":"10.1007/s10735-025-10560-x","url":null,"abstract":"<div><p>Extensive research has highlighted the involvement of excessive oxidative stress and pyroptosis in sepsis-caused acute lung injury (ALI). The present investigation delves into the potential role of Monoamine oxidase A (MAO-A) in this pathological process. Analyzing Gene Expression Omnibus (GEO) datasets alongside clinical samples revealed a significant upregulation of MAO-A in sepsis patients. To further elucidate this, cecal ligation puncture (CLP)-induced ALI were established in C57BL/6 mice. Additionally, human alveolar epithelial cells (HPAEpiC) treated with MAO-A inhibitor RO11-11639 were subjected to lipopolysaccharide (LPS) stimulation in vitro. The <i>in-vivo</i> experiments demonstrated that RO11-11639 mitigated CLP-induced ALI, significantly reducing pulmonary oxidative stress, inflammation and pyroptosis in lung tissue. Biochemical quantification revealed significant suppression of both oxidative stress biomarkers reactive oxygen species (ROS), malondialdehyde (MDA) and key inflammatory markers interleukin (IL)-1β, IL-16. Consistent with these findings, the <i>in-vitro</i> model confirmed that RO11-11639 reduced ROS and MDA accumulation, and inflammation in HPAEpiC, in response to LPS stimulation. Moreover, functional rescue analysis delineated the nuclear factor erythropoietin-2-related factor 2/heme oxygenase 1 (Nrf2/HO-1) pathway as the critical mediator of RO11-11639’s dual antioxidant and anti-pyroptosis activities in HPAEpiC. Mechanistically, MAO-A inhibition promoted the nuclear translocation of Nrf2, thereby activating the downstream regulatory proteins HO-1, quinone oxidoreductase 1 (NQO-1) and glutathione s-transferase (CST). These data cumulatively indicate that pharmacological targeting of MAO-A may offer therapeutic benefits in septic ALI by attenuating pathophysiological processes involving oxidative damage and inflammasome-mediated pyroptosis.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145037301","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":"Knockdown of circ_0000372 elevates PD-L1 level through sponging miR-488-3p to restrain cell viability, motility and immune escape in gastric cancer","authors":"Chao Shen,&nbsp;Wei Li,&nbsp;Ji Shi,&nbsp;Yan Wu,&nbsp;Yichao Yan","doi":"10.1007/s10735-025-10598-x","DOIUrl":"10.1007/s10735-025-10598-x","url":null,"abstract":"<div><p>Gastric cancer (GC) development is influenced by crosstalk between tumor cells and host immune elements. Circ_0000372 has potential as an oncogene. This research aimed to investigate the circ_0000372 mechanism in GC. Circ_0000372 expressions were evaluated via the GSE194384 database. The overall survival of GC patients was determined via the Kaplan-Meier Survival Curve. Gene relationships were assessed using the Chi-square test. Circ_0000372 functions in GC were evaluated with qRT-PCR, Cell Counting Kit-8 analysis, 5-ethynyl-2’-deoxyuridine analysis, Transwell, Western blot, co-culture of peripheral blood mononuclear cells (PBMCs) and GC cells, flow cytometry, and ELISA. Meanwhile, the circ_0000372 mechanism was examined by RNA pull-down, dual-luciferase reporter assay, and Spearman Correlation Analysis. Finally, the circ_0000372 impact <i>on</i> tumor-bearing mice was analyzed by immunohistochemistry and western blot assays. Elevated circ_0000372 levels were detected in GC. Patients with raised circ_0000372 levels had a poor prognosis. Besides, circ_0000372 expressions were interrelated to TNM stage and lymph node metastasis. Silencing circ_0000372 repressed GC cell proliferation and invasion. Silencing circ_0000372 reduced immune escape with reduced PD-L1 protein levels and increased CD8 + T cell percentage. Moreover, circ_0000372 positively regulated PD-L1 expression via miR-488-3p, and circ_0000372 knockdown restrained GC cell proliferation, invasion, and immune escape by derepressing PD-L1 via sponging miR-488-3p. The interference of circ_0000372 also reduced GC tumor formation, tumor weight, and PD-L1 level with elevated IFN-γ level in vivo. A high circ_0000372 level indicated a GC poor prognosis. Silencing circ_0000372 suppressed cell proliferation, invasion, and immune escape by derepressing PD-L1 via sponging miR-488-3p.</p><h3>Graphical abstract</h3><div><figure><div><div><picture><source><img></source></picture></div><div><p>Mode pattern of circ_0000372/miR-488-3p/PD-L1 in mediating GC cell proliferation, invasion, immune escape</p></div></div></figure></div></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145037304","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":"DLGAP5 facilitates glioblastoma growth and tumor-associated macrophage M2 polarization","authors":"Fujun Chen,&nbsp;Yong Luo,&nbsp;Fenghong Lv,&nbsp;Hongmin Li","doi":"10.1007/s10735-025-10592-3","DOIUrl":"10.1007/s10735-025-10592-3","url":null,"abstract":"<div><p>Human discs large-associated protein 5 (DLGAP5), also known as DLG7, is a crucial protein associated with the mitotic spindle and is increased in different types of tumours. Nevertheless, its role in glioblastoma (GBM) remain poorly understood. Therefore, the purpose of this work was to examine the mechanisms and biological functions of DLGAP5 in GBM. Furthermore, we investigated how DLGAP5 affected the polarisation of tumor-associated macrophages (TAMs). We assessed the growth, migration, and invasion of GBM cells using a cell counting kit (CCK8), 5-Ethynyl-2’-deoxyuridine (EdU) incorporation, wound healing, and Transwell assays. The expression levels of TAM-associated differentiation markers CD68, CD206, and CD11b were examined by flow cytometry. The effects of tumour cell-derived DLGAP5 on THP-1 macrophage polarisation were investigated using a coculture paradigm including GBM cells and differentiated THP-1 cells. The effect of DLGAP5 on carcinogenesis in vivo was also investigated using a xenograft nude mice model. DLGAP5 was found to be upregulated in both GBM tissues and cell lines. The knockdown of DLGAP5 inhibited GBM cell proliferation, migration, and invasion, as well as M2 polarization of TAMs. In an in vivo model, suppression of DLGAP5 led to decreased tumor growth. Our findings indicate that DLGAP5 significantly promotes the malignant phenotype of GBM. These findings have potential implications for the future diagnosis and therapy of GBM.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145037303","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":"Neuroprotection in neonatal Hypoxia-ischaemia: melatonin targets NCX1 to inhibit mitochondrial autophagy via the PINK1-Parkin pathway","authors":"Tongfei Cheng,&nbsp;Shanlong Du,&nbsp;Yi Cao,&nbsp;Ziyan Lu,&nbsp;Yingjun Xu","doi":"10.1007/s10735-025-10601-5","DOIUrl":"10.1007/s10735-025-10601-5","url":null,"abstract":"<div><h3>Objective</h3><p>Hypoxic ischaemic (HI) damage is a major cause of white matter damage (WMD) in the brains of newborns, especially preterm infants; early neuroprotection is essential to improve cognitive outcomes. This study aimed to investigate the effect of melatonin on nerve injury by inhibiting mitochondrial autophagy.</p><h3>Methods</h3><p>We established a neonatal WMD model through HI induction in postnatal day 3 (P3) Sprague–Dawley (SD) rats. Following four days of intraperitoneal melatonin administration (10 mg/kg/d), temporal changes in expression of sodium-calcium exchanger 1 (NCX1), myelin integrity markers (myelin-associated glycoprotein [MAG]/proteolipid protein [PLP]), and mitophagy-related proteins (microtubule-associated protein 1 light chain 3β [LC3β], PTEN-induced kinase 1 [PINK1], and Parkin RBR E3 ubiquitin-protein ligase [Parkin]) were systematically quantified. Neuronal hyperexcitability was evaluated by whole-cell patch-clamp recordings, whereas myelin pathology was assessed by luxol fast blue (LFB) staining, and mitochondrial ultrastructures were evaluated by transmission electron microscopy. Cognitive recovery was determined using Morris water maze testing at postnatal day 28.</p><h3>Results</h3><p>Our results demonstrated that rats subjected to HI presented biphasic alterations in NCX1 expression, characterised by transient upregulation on day 7 followed by a progressive decline (<i>P</i> &lt; 0.001). Concurrently, expression of mitochondrial autophagy markers (LC3β, PINK1, and Parkin) was significantly increased (<i>P</i> &lt; 0.001). Histological analysis revealed distinct mitochondrial structural damage and autophagosome formation. Electrophysiological measurements revealed increased neuronal excitability (<i>P</i> &lt; 0.05), which was correlated with spatial learning and memory deficits. Although melatonin treatment effectively attenuated these pathological alterations, subsequent pharmacological inhibition of NCX1 via SN6 administration in melatonin-treated rats resulted in the recurrence of mitochondrial ultrastructural abnormalities and the reactivation of autophagic pathways.</p><h3>Conclusion</h3><p>Melatonin attenuated activation of the PINK1-Parkin-dependent mitochondrial autophagy pathway in neonatal rats with HI-induced WMD through mediating the dynamic expression of NCX1. This intervention effectively reduced neuronal hyperexcitability, ameliorated demyelinating lesions, and improved long-term learning and cognitive functions.</p><h3>Clinical trial registration</h3><p>Not applicable.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-025-10601-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145037302","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":"BRAF mutations in ovarian cancer: immune microenvironment and therapeutic advances","authors":"Yuhang Wang,&nbsp;Xue Du","doi":"10.1007/s10735-025-10597-y","DOIUrl":"10.1007/s10735-025-10597-y","url":null,"abstract":"<div><p>Ovarian cancer is a highly lethal malignancy of the female reproductive system, characterized by a poor prognosis and complex therapeutic challenges influenced by various molecular and microenvironmental factors. Among these, mutations in the <i>BRAF</i> gene have received increasing attention across multiple malignancies due to their involvement in oncogenic signaling pathways and implications for targeted therapy. Concurrently, the tumor immune microenvironment has been recognized as a critical determinant in the initiation and progression of tumors. This review explores the impact of <i>BRAF</i> mutations on the immune microenvironment in ovarian cancer, summarizes recent advances in the field, and assesses the potential clinical significance of these findings in informing therapeutic strategies.</p><p>\u0000 \u0000 <i>Clinical trial number</i>: Not applicable.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145037364","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":"Antitumor effects of Dadas Cress (Lepidium sativum var. sativum) on Ehrlich Ascites tumor cells: an in vitro and in vivo study","authors":"Demet Ünalmış Aykar,&nbsp;Harun Ülger,&nbsp;Züleyha Doganyiğit,&nbsp;Gökçe Şeker Karatoprak,&nbsp;Dilek Pandır,&nbsp;Sümeyye Uçar,&nbsp;Emin Kaymak,&nbsp;Aslı Okan Oflamaz,&nbsp;Seher Yılmaz","doi":"10.1007/s10735-025-10575-4","DOIUrl":"10.1007/s10735-025-10575-4","url":null,"abstract":"<div><p>Garden cress (Lepidium sativum L.) is widely used in nutrition and traditional medicine for its bioactive properties. Studies show its seeds and leaves have anticancer, antimicrobial, and antidiabetic effects. This study investigated the antitumor potential of an extract from the leaves of Dadaş cress (<i>Lepidium sativum</i> var. <i>sativum</i>), a Turkish variety, against Ehrlich Ascites Tumor (EAT) cells. In the in vitro study, Dadaş cress extract (DCE) was tested at 25, 50, and 100 µg/mL concentrations to evaluate its antitumor activity. Caspase-3/7 activity was measured by fluorometric assay, mitochondrial membrane depolarization by JC-1 dye, and cell cycle by flow cytometry. The 50 µg/mL group had the highest apoptosis rate at 48 h; 100 µg/mL caused the most mitochondrial depolarization at 24 h. After 72 h, the 5-FU group had the highest G0/G1 phase cells, while the 25 µg/mL DCE group had the highest S phase cells. In vivo, groups were control, EAT control, EAT + 5-FU, EAT + DCE (75–150 mg/kg), and DCE only (75–150 mg/kg). Liver and kidney tissues were examined immunohistochemically, biochemically, and genotoxically. DCE significantly lowered TNF-α expression, oxidative stress, and DNA damage in EAT mice. In the 150 mg/kg DCE group, renal tail DNA% dropped from 92.5 to 34.8%, liver tail DNA% from 105.3 to 65.8%. TAS increased, TOS decreased vs. EAT control (<i>p</i> &lt; 0.05). These results suggest DCE protects against EAT-induced damage dose-dependently and has no genotoxicity. The findings suggest that DCE may have antitumor potential.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 5","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145037367","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}