Journal of Molecular Histology最新文献

{"title":"Mesenchymal stem cell exosomes regulate TGFβ/Smad3 by decreasing the METTL3-NEAT1 axis to inhibit scar progression after breast surgery","authors":"Juan Du,&nbsp;Jincheng Wu,&nbsp;Qinqin Song,&nbsp;Shuangru Li,&nbsp;Youwang Hong,&nbsp;Aizaz Anwar,&nbsp;Quanyou Fu,&nbsp;Jisong Liu","doi":"10.1007/s10735-025-10441-3","DOIUrl":"10.1007/s10735-025-10441-3","url":null,"abstract":"<div><h3>Background</h3><p>Scars are traces of tissue loss left behind by connective tissue overgrowth and repair. Studies in recent years have shown that mesenchymal stem cell exosomes (MSC-Exo) have the ability to inhibit and repair cutaneous scarring, but their specific role in post-breast surgery scar formation and the mechanisms behind it remain enigmatic.</p><h3>Methods</h3><p>Extraction and characterization of exosomes from mesenchymal stem cells (MSCs). Western Blot and RT-qPCR were used to evaluate the expression of fibrillar protein and TGF-β/Smad3 in mammary hypertrophic scar fibroblasts (MHSFs) stimulated with MSC-Exo, sh-METTL3, sh-NEAT1 and their negative controls. Construction of a mouse model of proliferative scar formation using mechanical tension and detection of fibronectin and pathway protein expression using Western Blot and RT-qPCR. Pathologic changes of mammary scarring in mice using HE staining, Masson staining and immunofluorescence.</p><h3>Results</h3><p>Both in vitro and in vivo, MSC-Exo, sh-METTL3 and sh-NEAT1 were shown to decrease the expression of COL1A1, COL3A1, α-SMA, fibronectin, TGF-β, p-Smad2/Smad2, p-Smad3/Smad3, by Western Blot and RT-qPCR. In addition, improved lesions and reduced collagen deposition were observed in mice by HE and Masson assays.</p><h3>Conclusions</h3><p>In summary, our study revealed that exosomes of MSCs function through the m6A methyltransferase METTL3, which regulates the NEAT1/TGF-β/Smad3 axis to slow down the rate of scar formation after breast surgery.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144090976","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":"Arsenic-induced neurocardiac toxicity and protective role of Resveratrol: histopathological and molecular insights","authors":"Saroj,&nbsp;Kamakshi Mehta,&nbsp;Kamlesh Kumar Pandey,&nbsp;Balpreet Kaur,&nbsp;Saroj Kaler,&nbsp;Pushpa Dhar","doi":"10.1007/s10735-025-10439-x","DOIUrl":"10.1007/s10735-025-10439-x","url":null,"abstract":"<div><p>Arsenic toxicity is a global health problem chiefly targeting soft tissues of the body like the brain and heart. The major mechanism underlying arsenic-induced neurotoxicity is oxidative stress. Particularly, the neurons and cardiac myocytes show limitless susceptibility to oxidative stress. Herein, we examined the impact of prolonged arsenic exposure and resveratrol post-treatment on the cardiac and neuronal [Ventromedial hypothalamic nucleus (VMH)] morphology. Adult mice were segregated into control and experimental groups; controls received distilled water, while experimental groups received oral gavage of arsenic trioxide (ATO) at low (2 mg/kg bw) or high (4 mg/kg bw) doses for 45 days. Cardiac effects were assessed at the low dose (2 mg/kg bw), whereas neurological effects were evaluated at both low and high doses. Mice were sacrificed on day 45 to obtain perfusion-fixed hearts and brains for histological and morphometric studies. Long-term ATO exposure resulted in a higher heart-to-body weight ratio than controls, suggesting ATO-induced hypertrophy. Microscopic observations revealed a regular arrangement of cardiac muscle fibres, branching patterns of cardiomyocytes, and fibroblasts across all the treatment groups. However, increased cardiac myocyte diameter in ventricles and substantial fibrosis in vessel walls were noticed in ATO-alone exposed hearts relative to controls. Selective vulnerability of hypothalamic neurons following ATO exposure was evident by significant alterations in morphometric parameters (reduced cell density and soma size) in the VMH nucleus of animals receiving ATO (2 and 4 mg/kg) alone. These dramatic histopathological alterations were found to be restored after ATO + <i>Res</i> co-treatment. We also examined the expression of ER-α in the preoptic area of the hypothalamus and indicated downregulation of ER-α due to prolonged ATO exposure. Our findings highlight Resveratrol as a potent neurocardiac protector against ATO toxicity via estrogen signaling modulation, supporting its therapeutic potential in arsenic poisoning.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144090977","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":"Exploring neuro-glial interaction mechanisms in myelin plasticity for learning and memory enhancement","authors":"Reham M. Wahid,&nbsp;Nancy Husseiny Hassan,&nbsp;Walaa Samy,&nbsp;Aliaa Talaat,&nbsp;Amira Mokhtar Gobran,&nbsp;Shaimaa R. Abdelmohsen,&nbsp;Heba Atef Elsayed","doi":"10.1007/s10735-025-10431-5","DOIUrl":"10.1007/s10735-025-10431-5","url":null,"abstract":"<div><p>Neural plasticity was considered as the principal mechanism for learning and memory many decades ago. So our study aims to figure out the underlying mechanisms of myelin plasticity associated with learning and memory. Myelin was considered for a long time as static, inert insulator, irrelevant to learning. But recent studies showed that myelination is dynamically changed to enhance neuronal plasticity. The study was conducted on 24 rats, divided into 3 groups, with 8 rats in each: Group 1: control in cages; Group 2: control untrained; and Group 3: rats were trained using Barnez maze behavior test. The gene expression analysis for <i>Sox10</i>, <i>Myrf</i>, <i>Nrg1</i>, <i>Bdnf</i>, <i>Serpine2</i> and <i>Mbp</i> was evaluated by qRT-PCR in hippocampus tissues with correlation assessment, and histopathological and immunohistochemistry assessment were done. The present study showed improved spatial memory with increased myelination in the trained group, in addition to high expression of <i>Sox10</i>, <i>Myrf</i>, <i>Nrg1</i> and <i>Bdnf</i> in the trained group compared to all others (<i>P</i> &lt; 0.001). <i>Serpine2</i> and <i>GFAP</i> as markers of astrocytes showed high expression in the trained group in comparison with other groups (<i>P</i> &lt; 0.001) with strong positive correlation between <i>Serpine2</i> and <i>Mbp</i> (r = 0.76, <i>P</i> = 0.02). Myelin plasticity as one of the crucial learning mechanisms, was influenced by different neural and environmental signals. In addition, there was a significant role of astrocytes in promoting such myelination effect.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144091181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A diet-driven metabolic dysfunction-associated steatohepatitis (MASH) mouse model resembles the corresponding human disease","authors":"Guilherme Ribeiro Romualdo,&nbsp;Letícia C. Valente,&nbsp;Gabriel P. Bacil,&nbsp;Luana Riechelmann-Casarin,&nbsp;Antônio R. B. da Fonseca,&nbsp;Miguel W. Fornes,&nbsp;Luís F. Barbisan","doi":"10.1007/s10735-025-10449-9","DOIUrl":"10.1007/s10735-025-10449-9","url":null,"abstract":"<div><p>Most of the available preclinical Metabolic dysfunction-associated steatotic liver disease (MASLD) and steatohepatitis (MASH) models fail to resemble metabolic comorbidities and liver fibrosis. To establish a standard MASLD/MASH model, we characterized some morphological, biochemical, and transcriptomic features in a Western diet-induced MASLD model in mice, depicting its similarities to the corresponding human disease. Male C57BL/6J mice received a hypercaloric diet containing sucrose, saturated fat, and cholesterol-rich chow, and high sugar solution for 24 weeks. This model featured a distinct MASH phenotype with obesity, impaired glucose metabolism, hypercholesterolemia, extensive macro and microvesicular, liver steatosis, and slight-to-moderate pericellular/perisinusoidal fibrosis, which was in keeping with the increased hepatic levels of IL-6 and TNF-α, and upregulation of 18 collagen subunit genes (as <i>Col1a1</i>, <i>Col1a2</i>, <i>Col3a1</i>, <i>Col5a2</i>, <i>Col4a1</i>, <i>Col6a3</i>, <i>Col14a1</i>, <i>Col6a2</i>, <i>Col5a1</i>), 34 cytokines or chemokines or related receptors-coding genes (as <i>Il15</i>, <i>Cxcl9</i>, <i>Ccl22</i>), 18 TNF-related genes (as <i>Tnfaip8l3</i>, <i>Tnfrsf21</i>, <i>Tnfaip8</i>, <i>Tnfrfs12a</i>) and 12 metalloproteinase/tissue inhibitors of metalloproteinases-related genes (as <i>Mmp2</i>, <i>Mmp7</i>). The downregulated genes were negative regulators of gluconeogenesis, insulin secretion, and lipid biosynthesis, most belonging to the major urinary protein (MUP) family. The computational analysis of human samples revealed a similarity between our bioassay and human steatohepatitis, with the upregulation of fibrosis- and inflammation-associated orthologs (<i>COL1A1</i>, <i>COL1A2</i>, <i>COL3A1</i>, <i>COL5A2</i>, <i>COL4A1</i>, <i>COL6A3</i>, <i>COL14A1</i>, <i>COL6A2</i>, <i>COL5A1</i>, <i>TNFAIP8L3</i>, <i>TNFRSF21</i>, <i>TNFAIP8</i>, <i>TNFRFS12A</i>, <i>IL15</i>, <i>CXCL9</i>, <i>CCL22</i>, <i>MMP2</i>, <i>MMP7</i>). Our mouse model may be applied as a standard MASH translational bioassay, providing valuable insights into the inflammatory/fibrosis axis of this chronic disease, from the pathogenesis to therapeutic intervention.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144090975","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":"Dysregulated autophagy in periodontal ligament stem cells of individuals with type 2 diabetes mellitus and periodontitis","authors":"Qian-Qian Chen,&nbsp;Jie Huang,&nbsp;Qi Liu,&nbsp;Kun Yang","doi":"10.1007/s10735-025-10455-x","DOIUrl":"10.1007/s10735-025-10455-x","url":null,"abstract":"<div><p>This study aimed to investigate autophagy and its associated mechanisms in periodontal ligament stem cells (PDLSCs) within the inflammatory microenvironment of type 2 diabetes mellitus (T2DM) and periodontitis. Periodontal ligament tissues were obtained from healthy individuals, individuals with T2DM, individuals with chronic periodontitis, and individuals with both T2DM and periodontitis. PDLSCs were isolated, cultured, and treated with the autophagy inhibitor 3-methyladenine (3-MA) and the autophagy activator rapamycin (Rapa). Cell proliferative capacity was evaluated, autophagic activity and organelle damage were assessed using transmission electron microscopy, and the relative expression levels of autophagy-related genes (<i>Beclin-1</i>,<i> LC3 II</i>,<i> P62</i>) were measured using real-time quantitative PCR. Compared to PDLSCs derived from healthy individuals, those from individuals with chronic periodontitis or T2DM exhibited no significant morphological differences but demonstrated reduced proliferative capacity. Treatment with 3-MA and Rapa did not significantly alter proliferative capacity across groups. PDLSCs from individuals with chronic periodontitis and T2DM displayed increased autophagosome formation, more severe organelle damage, and upregulated expression of autophagy-related genes <i>Beclin-1</i> and <i>LC3 II</i>, while P62 expression was downregulated, compared to PDLSCs from healthy individuals. PDLSCs from individuals with T2DM and periodontitis exhibit excessive autophagy and organelle damage. Autophagy dysregulation in PDLSCs within a diabetic and inflammatory microenvironment may contribute to the severity of periodontal destruction observed in individuals with T2DM.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144090974","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":"Effect of autologous cytokine-rich serum and platelet-rich plasma administration on oxidative status, minerals and proinflammatory cytokines in brain and serum in cyclophosphamide-induced ovarian failure","authors":"Mustafa Ermiş,&nbsp;Erol Karakaş,&nbsp;Hanifi Erol,&nbsp;Gökhan Akcakavak,&nbsp;Recai Aci,&nbsp;Furkan Ümit,&nbsp;Özhan Karatas,&nbsp;Gülay Çiftci","doi":"10.1007/s10735-025-10448-w","DOIUrl":"10.1007/s10735-025-10448-w","url":null,"abstract":"<div><p>Cyclophosphamide (CP) is one of the most commonly used chemotherapy agents and carries a high risk of ovarian damage. This study aimed to evaluate the effects of autologous cytokine-rich serum (ACRS) and platelet-rich plasma (PRP) on brain oxidative status, mineral levels, and proinflammatory cytokines in rats with CP-induced ovarian failure. A total of 42 female Wistar rats (12-weeks-old) were used in the study. Six of these rats were allocated as donors, and the remaining 36 rats were randomly distributed into six groups (n = 6 per group). Group 1 received no treatment. On the 1st and 7th days, 75 mg/kg of CP was administered intraperitoneally to Groups 4, 5, and 6. On day 1, PRP was administered intraovarianly to Groups 2 and 5, while ACRS was administered intraovarianly to Groups 3 and 6. Additionally, PRP and ACRS were administered intraperitoneally to the respective groups on 7th and 14th days.The study was terminated at the end of the 31st day. Brain tissue and blood samples were collected for biochemical analyses and ovarian tissue samples were collected for histomorphological examinations. Morphological analysis using Hematoxylin–Eosin (HE) staining and immunohistochemical evaluation for AMH, α-SMA, and IL-1β were conducted on the ovaries. Proinflammatory cytokines and insulin levels were measured using ELISA test kits. TAS/TOS levels were assessed using Relassay Diagnostic kits. Biochemical parameters and mineral levels were measured using autoanalyzer. Histopathological evaluation revealed that follicular degeneration, congestion, hemorrhage, edema, and inflammatory cell infiltration, as well as the number of atretic follicles and IL-1β immunoreactivity, were observed at the highest levels in the CP group (Group 4). In contrast, the numbers of primordial, primary, secondary, and tertiary follicles, along with AMH and α-SMA immunoreactivity levels, were found to be the lowest in this group. However, positive therapeutic effects were observed in the CP-treated groups (Groups 5 and 6). In the serum, increased levels of AST, ALT, creatinine, glucose, LDL, TOS, Ca, Fe, Mg, IL-1β, IL-1α, TNF-α, and NF-kB were detected in the CP groups (G4, G5, G6) compared to the control groups (G1, G2, and G3). In brain tissue, a decrease of total protein and total cholesterol levels were observed in the CP groups (G4, G5, G6) compared to the control groups, while increases in Na, Cl, Fe, IL-1β, IL-1α, TNF-α, and NF-kB levels were detected. In conclusion, PRP and ACRS therapies from the patient's own blood have a potential as supportive or chemopreventive strategies with reduced side effects and treatment costs.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144084810","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":"Activation of Hippo/YAP signaling pathway exacerbates vascular remodeling and aggravates hypertension by upregulating Foxm1","authors":"Jing Bai,&nbsp;Yujuan Yang","doi":"10.1007/s10735-025-10443-1","DOIUrl":"10.1007/s10735-025-10443-1","url":null,"abstract":"<div><p>The Hippo/YAP signaling pathway is closely related to the occurrence and development of cardiovascular diseases. However, it’s still unclear whether this pathway plays a certain role in hypertension. In this study, aortic morphology and function in spontaneously hypertensive rats (SHR) were comprehensively evaluated using Wistar-Kyoto rats (WKY) as controls. Results indicated that the aorta of SHRs have distinct changes in pathological structure. Furthermore, the proliferative activity of vascular smooth muscle cells (VSMCs) was enhanced, with vascular fibrosis being aggravated. Immunohistochemical analysis revealed that SHRs exhibited high expression of Yes-Associated Protein (YAP). Western Blot analysis showed that cytoplasmic YAP and TAZ expression decreased in hypertensive rats, indicating that YAP/TAZ nuclear transfer increased and Hippo/YAP signaling pathway had been activated. The cell function experiments of VSMCs extracted from rat aorta showed that the cell viability and proliferation ability of VSMCs in SHRs were enhanced, the expression of Fibronectin and collagen I was increased, and vascular fibrosis was aggravated. siRNA-YAP (si-YAP) can reverse the above phenomenon in VSMCs. Knockdown of YAP can inhibit Foxm1 expression. As an inhibitor of large tumor suppressor kinases LAST1/2, GA-107 can inhibit the phosphorylation level of YAP, increase blood pressure, aggravate aortic pathomorphological changes, promote VSMCs proliferation and vascular fibrosis, and thus aggravate hypertension symptoms in SHRs. However, these effects of GA-107 can be antagonized by inhibiting Foxm1 with thiosulfathiazole (Thio). Conclusively, Hippo/YAP signaling pathway promotes vascular remodeling through the regulation of Foxm1 and causes hypertension.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144084808","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":"Evaluation of the protective effects of raw and roasted pumpkin (Cucurbita pepo L.) seed-supplemented diets on cisplatin-induced cardiotoxicity in rats","authors":"Seun Funmilola Akomolafe,&nbsp;Moses Orimoloye Akinjiyan,&nbsp;Nnaemeka Tobechukwu Asogwa,&nbsp;Olusola Olalekan Elekofehinti","doi":"10.1007/s10735-025-10432-4","DOIUrl":"10.1007/s10735-025-10432-4","url":null,"abstract":"<div><p>Cardiovascular diseases are among the top killer diseases globally. This work assessed the cardioprotective ability of raw and roasted pumpkin (<i>Cucurbita pepo</i> L.) seed-supplemented diets on cisplatin-induced heart damage in rats. The cardiotoxicity was induced with cisplatin (7 mg/kg) intraperitoneally. The rats’ six groups were treated for 14 days: control rats fed a normal diet; group 2: cisplatin-induced (CIS) untreated; groups 3 and 4: CIS + 5% raw pumpkin seed (RW) and CIS + 10% RW; groups 5 and 6: CIS + 5% and 10% roasted pumpkin seed (RT). The biochemical assays were done using standard procedures, and Schrödinger suites were used for in silico studies of <i>C. pepo</i> phytocompounds with phosphodiesterase 5. There was a significant (<i>p</i> &lt; 0.05) elevation in arginase, phosphodiesterase-5, adenosine deaminase, acetylcholinesterase, and butyrylcholinesterase activities, ROS and TBARS in cisplatin-induced rats relative to control. Cisplatin-induced rats also have their nitric oxide, antioxidant (catalase, GST, and GSH) levels reduced, and the heart’s histoarchitectural structure degenerated relative to control. These conditions were reversed upon treatment with raw and roasted pumpkin seeds (5% and 10%). Molecular docking of <i>C. pepo</i> phytocompounds like chlorogenic acid (-11.4 kcal/mol), beta-sitosterol (-11.013 kcal/mol), quercetin (-10.323 kcal/mol), and epicatechin (-10.168 kcal/mol) suggests that they are potent inhibitors of phosphodiesterase 5, better than standard drug pravastatin (-9.809 kcal/mol), with a good pharmacotoxicity profile. The study suggests that the cardioprotective effect of raw and roasted pumpkin seeds could be via their ability to inhibit phosphodiesterase 5, improve vasodilation, increase antioxidant levels, and alleviate oxidative stress.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144084809","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":"Field Marigold (Calendula arvensis L.) accelerates wound-healing in vivo: role of transforming growth factor-beta1 (TGF-β1), inflammatory, and biochemical molecules","authors":"Safwan Mahmoud Al-Adwan,&nbsp;Talal Salem Al-Qaisi,&nbsp;Ahmed A.j. Jabbar,&nbsp;Kamaran Younis M. Amin,&nbsp;Hawri Fatih Sami,&nbsp;Hanan Ibrahim Althagbi,&nbsp;Ahmed Hameed Al-Dabhawi,&nbsp;Bassam Ali Abed Wahab,&nbsp;Rawaz Rizgar Hassan,&nbsp;Mahmood Ameen Abdulla,&nbsp;Musher Ismael Saleh","doi":"10.1007/s10735-025-10433-3","DOIUrl":"10.1007/s10735-025-10433-3","url":null,"abstract":"<div><p>Medicinal plants are major sources of natural products, which have gained a renewed interest in recent years because of drawbacks associated with synthetic ones used for human health disorders. <i>Calendula arvensis</i> L. is a traditional medicinal plant used for many inflammatory-related diseases. The study explores the acute toxicity and wound-healing effects of methanolic extracts of <i>Calendula arvensis</i> L. aerial parts (MECAA) on excisional neck injury in rats. A two-week acute toxicity procedure was applied to find the safety of MECAA in animal models. For the wound-healing experiment, a uniform dorsal neck injury was created for twenty-four Sprague–Dawley rats, which were aligned arbitrarily into 4 groups and received topical treatments; group A rats addressed with normal saline; group B rats had intrasite gel; groups C and D rats had 0.2 ml of 250 and 500 mg/kg of MECAA, respectively. There was no toxicity nor mortality in rats supplemented orally with up to 5 g/kg MECAA. MECAA topical addressing accelerated wound contraction represented by higher deposition of fibroblast and keratinocytes, angiogenic factors, and reduced inflammatory cells. MECAA treatment up-regulated tissue antioxidants (SOD and CAT), transforming growth factor-β 1, and hydroxyproline (collagen) contents while lowering MDA and serum inflammatory mediators (TNF-α and IL-6). The outcomes can serve as scientific evidence for the traditional use of <i>Calendula arvensis</i> as a wound healer, which requires further molecular isolation and identification as a viable source of a potent drug formulation.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144074025","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":"Downregulation of MPC1 promotes HCC cell proliferation and metastasis via the STAT3 pathway","authors":"Dandan Shan,&nbsp;Qiuxian Zheng,&nbsp;Zhi Chen","doi":"10.1007/s10735-025-10435-1","DOIUrl":"10.1007/s10735-025-10435-1","url":null,"abstract":"<div><p>Hepatocellular carcinoma (HCC) is prevalent globally, and the discovery of new targets is vital for the treatment of HCC. Mitochondrial pyruvate carrier 1 (MPC1) has been found to exhibit reduced expression and promote tumour progression in some cancers, although its role in HCC needs to be explored. Using GEO datasets and Kaplan‒Meier plotter, the clinicopathological features and patient prognosis were analysed by assessing the expression levels of MPC1 in HCC tissues. After MPC1-knockdown and MPC1-overexpressing cell lines were constructed, the effects of modulating MPC1 expression on the malignant phenotype of HCC cells were tested via CCK8, colony formation, and scratch assays and flow cytometry. The effects of MPC1 on HCC cells and mitochondria were examined via MitoTracker Red CMXRos staining, cytoskeleton staining and cellular energy metabolism assays. MPC1 expression was found to be reduced in HCC patients and correlated with prognosis and clinicopathological features. It was found that low expression of MPC1 promotes the malignant phenotype of HCC cells and affects the mitochondrial energy metabolism of HCC cells to support the tumour microenvironment, and that MPC1 may act through signal transducer and activator of transcription 3 (STAT3). MPC1 might play a tumor-suppressing role in HCC through its interaction with STAT3, and this discovery could offer novel perspectives for HCC treatment.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143949654","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}