Tissue & cell最新文献

{"title":"Dimethyloxalylglycine regulates osteogenesis of dental pulp stem cells through PI3K/AKT signaling pathways","authors":"Qiannan Dong ,&nbsp;Hengwei Zhang ,&nbsp;Qian Zhang ,&nbsp;Xiuzhi Fei ,&nbsp;Jianping Ruan ,&nbsp;Longlong He","doi":"10.1016/j.tice.2025.103012","DOIUrl":"10.1016/j.tice.2025.103012","url":null,"abstract":"<div><h3>Background</h3><div>Dental pulp mesenchymal stem cells (DPSCs) are typically cultivated in vitro under normoxic conditions, which may adversely affect their biological functions during research and treatment. Dimethyloxalylglycine (DMOG) is a small-molecule drug that has demonstrated impressive therapeutic outcomes in conditions such as osteoporosis.</div></div><div><h3>Objective</h3><div>However, the influence of DMOG on the osteogenesis associated with DPSCs remains inadequately understood. We propose that DMOG may significantly impact the biological functions related to osteogenesis in DPSCs when exposed to normoxic conditions.</div></div><div><h3>Materials and methods</h3><div>DPSCs were obtained through tissue block enzyme digestion. Tube formation experiment was conducted, quantitative polymerase chain reaction (qPCR) was employed to assess the angiogenic activity of DPSCs. Additionally, alkaline phosphatase (ALP) activity tests, alizarin red staining (ARS), qPCR and western blotting (WB) assays were utilized to evaluate the osteogenic activity of DPSCs. The proposed mechanism was confirmed through repeated experiments.</div></div><div><h3>Results</h3><div>DMOG significantly influences the osteogenic functions of DPSCs under normoxic conditions. Our findings further confirm that DMOG stimulates the phosphatidylinositol 3-kinase (PI3K)/Protein kinase B (AKT) signaling pathway in DPSCs via phosphorylation. Inhibition of this pathway can partially impede the biological effects of DPSCs related to osteogenesis and angiogenesis.</div></div><div><h3>Conclusion</h3><div>We have addressed the gap in understanding the effect of DMOG on the osteogenesis of DPSCs. Unlike previous studies that examined the regulation of osteogenesis in stem cells by DMOG, our findings suggest that a lower dose of DMOG is sufficient to enhance the osteogenesis of DPSCs. This could represent a promising strategy for cellular therapy in bone regeneration.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 103012"},"PeriodicalIF":2.7,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144270716","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":"Expression and biological activity of a novel protein species from cementum","authors":"Lia Hoz-Rodríguez ,&nbsp;Gonzalo Montoya-Ayala ,&nbsp;Oscar Vivanco-Rojas ,&nbsp;Enrique Romo-Arévalo ,&nbsp;Karina Jiménez-Durán ,&nbsp;Sonia López-Letayf ,&nbsp;Margarita Zeichner-David ,&nbsp;Maricela Santana Vázquez ,&nbsp;Higinio Arzate","doi":"10.1016/j.tice.2025.103004","DOIUrl":"10.1016/j.tice.2025.103004","url":null,"abstract":"<div><div>Cementum is a specialized mineralized connective tissue with singular histological and functional characteristics. Proteins isolated from human cementum appear to regulate periodontal ligament stem cells differentiation, help to maintain homeostasis and appear to control some of the molecular events required for periodontium formation, therefore emerging as novel therapeutic candidates for periodontal regeneration. The possibility that there might be cementum components, so far not described, was explored in these studies. This study reports the expression and biological activity of a novel human species from cementum termed cementogenin (CMGN). This molecule encodes a 195 aminoacid protein species with a predicted molecular mass of 20.2 kDa. Polyclonal antibodies against a GMGN’s selected peptide sequence were produced to identify the protein. Expression of CMGN in cells of the periodontium was examined by Western blot and immunofluorescence using histological sections of the periodontium. These studies revealed that CMGN is expressed by cementoblasts and cells of the periodontal ligament. Expression of CMGN’s mRNA and its protein in different periodontium cell types was determined by RT-qPCR and Western blot, respectively. CMGN mRNA and gene product levels were highly expressed by cementoblasts and osteoblasts cells. The CMGN protein was expressed in <em>E. coli</em> for functional studies using in vitro cell-free system. Assays revealed that <em>hr</em>CMGN promotes the nucleation of hydroxyapatite crystals. The human recombinant CMGN (<em>hr</em>CMGN) promoted cell proliferation, cell attachment, and differentiation by human periodontal ligament cells to a mineralized phenotype. Overall, our findings reveal that CMGN represents a new species isolated from cementum and might provide the basis for future studies that will allow further characterization of the structural features of CMGN and a better understanding of its functional properties. This new protein might be highly relevant in future periodontal therapeutics.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 103004"},"PeriodicalIF":2.7,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144270714","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":"SOX2OT inhibition enhances the choline O-Acetyltransferase gene expression in neuronal differentiation model of NT2 cells","authors":"Marie Saghaeian Jazi ,&nbsp;Soroush Akbar ,&nbsp;Saeed Mohammadi ,&nbsp;Lorena Zentilin","doi":"10.1016/j.tice.2025.103011","DOIUrl":"10.1016/j.tice.2025.103011","url":null,"abstract":"<div><h3>Objective</h3><div>This experimental study aimed to investigate the role of SOX2OT in NT2 cell neuronal differentiation to elucidate its specific function in this process, which remains unclear despite previous research highlighting its importance in central nervous system development.</div></div><div><h3>Material and methods</h3><div>We utilized the NT2 cell line to create a constitutive SOX2OT knocked-down cell clone (SNT2) and a control clone (LNT2) through lentivirus-mediated shRNA delivery. All cell types underwent 3 weeks of neuronal differentiation induced by retinoic acid. Assessment involved morphological changes, Tubulin BIII immunofluorescence staining, and qRT-PCR for gene expression, including SOX2OT and neuronal markers (Nestin, CHAT, GFAP), compared to the control.</div></div><div><h3>Results</h3><div>We demonstrated that stable SOX2OT inhibition did not hinder NT2 cell neuronal differentiation. SNT2 cells maintained their ability to morphologically differentiate into neurons, expressing Tubulin IIIB protein. Before differentiation, SNT2 cells showed a significant increase in CHAT expression (<em>p</em>-value = 0.01), persisting after 21 days (<em>p</em>-value = 0.037). While differentiation triggered a mild early decrease in SOX2OT expression in control cells, it increased in all cells during the third week. The neural differentiation lead to a general decrease in the gene expression of Nestin, and elevating trends in CHAT, and GFAP neuronal markers. By day 21, the expression of all genes in SNT2 cells significantly differed from NT2 controls (<em>p</em>-value = 0.037), suggesting SOX2OT's potential role in NT2 cell neuronal differentiation.</div></div><div><h3>Conclusion</h3><div>The results of this study showed that SOX2OT constitutive knocked down NT2 cells are still capable of differentiating into neuronal cells. However, SOX2OT inhibition can affect the expression of neuronal markers including choline O-Acetyltransferase which suggests its importance in the process of neuronal differentiation.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 103011"},"PeriodicalIF":2.7,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144270715","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":"3D traction force microscopy in human trabecular meshwork tissues: Effects of ROCK and YAP/TAZ inhibition in normal and glaucomatous tissues","authors":"Alireza Karimi ,&nbsp;Mini Aga ,&nbsp;Ansel Stanik ,&nbsp;Tia Harbaugh ,&nbsp;Elise Coffey ,&nbsp;Elizabeth White ,&nbsp;Mary J. Kelley ,&nbsp;Ted S. Acott","doi":"10.1016/j.tice.2025.103005","DOIUrl":"10.1016/j.tice.2025.103005","url":null,"abstract":"<div><div>Primary open-angle glaucoma (POAG) is the leading cause of irreversible blindness worldwide, with an estimated 112 million people projected to be affected by 2040. The primary risk factor for POAG is elevated intraocular pressure (IOP), which is primarily driven by increased resistance to aqueous humor outflow through the conventional outflow pathway. Despite its prevalence, the precise biomechanical mechanisms underlying this resistance remain unclear. In this study, we utilized 3D <em>in situ</em> traction force microscopy to investigate the effects of the rho kinase (ROCK) inhibitor Y-27632 and the YAP/TAZ inhibitor Verteporfin treatments on the trabecular meshwork (TM) and juxtacanalicular tissue (JCT) cellular contractility and their extracellular matrix (ECM) reorganization in both normal and glaucomatous human donor eyes. Our analysis revealed dysregulated traction forces within glaucomatous tissues, leading to significant ECM reorganization that may contribute to disrupting the homeostasis of the aqueous outflow pathway. Treatments appear to help restore normal ECM structure by adjusting cellular forces. The effect on contractile forces differed between genders, suggesting the significance of gender in treatment response. Our results suggest that targeting these biomechanical pathways may offer new therapeutic strategies to reduce outflow resistance, laying the groundwork for future therapies aimed at preserving vision by restoring ECM biomechanics and improving outflow.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 103005"},"PeriodicalIF":2.7,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144230986","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":"Linoleic acid induces migration and invasion through TLR4 in breast cancer cells","authors":"Kevin Perez Zaragoza,&nbsp;Rocio Castillo-Sanchez,&nbsp;Maria Sanchez-Juarez,&nbsp;Pedro Cortes-Reynosa,&nbsp;Eduardo Perez Salazar","doi":"10.1016/j.tice.2025.103009","DOIUrl":"10.1016/j.tice.2025.103009","url":null,"abstract":"<div><div>Breast cancer is the most diagnosed cancer and the leading cause of cancer-related deaths among worldwide women. Linoleic acid (LA) is an essential omega-6 polyunsaturated fatty acid and the most common polyunsaturated fatty acid in Western diets. Particularly, overweight and obesity are risk factors for breast cancer development in postmenopausal women. LA stimulates an elevation in PLD activity, as well as promotes migration and invasion in MDA-MB-231 breast cancer cells and an epithelial-to-mesenchymal transition process in MCF10A cells. Toll-like receptors (TLRs) are a group of type I transmembrane receptors that have been linked with cancer progression in various types of tumors, including breast cancer. TLR4 is expressed in immune cells, epithelial cells and breast cancer cells, and an inhibition of TLR4 expression in MDA-MB-231 cells promotes a decrease in their viability, proliferation and the secretion of IL-6 and IL-8. This study demonstrates that LA stimulates migration through TLR4 activity in MDA-MB-231 and MCF-7 breast cancer cells. Moreover, LA promotes FAK activation, focal adhesion assembly, an increase in MMP-9 secretion and invasion through TLR4 activity in MDA-MB-231 cells. Our findings demonstrate a signal transduction pathway in which LA activates FFAR1/FFAR4, which in turn activates TLR4 leading to the regulation of specific cellular processes, such as migration and invasion in breast cancer cells.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 103009"},"PeriodicalIF":2.7,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144241037","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":"OTUD5 enhances activation of multiple cell death pathways and hyperoxia-induced lung injury by stabilizing TRAF4 and activating the p38/JNK pathway","authors":"Xia Gu ,&nbsp;Tong Zhu ,&nbsp;Guihua Hang ,&nbsp;Wenjie Chen ,&nbsp;Huiping Chen","doi":"10.1016/j.tice.2025.103008","DOIUrl":"10.1016/j.tice.2025.103008","url":null,"abstract":"<div><h3>Objective</h3><div>This study aims to elucidate the role of OTUD5 in hyperoxia-induced lung injury and to explore its potential as a therapeutic target for mitigating oxidative stress-related lung damage.</div></div><div><h3>Methods</h3><div>AAV9-OTUD5 siRNA was administered via intratracheal injection in a mouse model to silence OTUD5 before exposure to 60 % O₂ for 24 h. Lung tissues were analyzed using histological techniques (HE, Masson’s, PAS staining) and quantified for collagen deposition and airway epithelial changes. Additionally, qPCR and WB analysisWB analysis assessed OTUD5 and TRAF4 expression levels. Co-immunoprecipitation and dual-immunofluorescence assays evaluated the interaction between OTUD5 and TRAF4. Apoptosis was measured via TUNEL staining and Cleaved-Caspase-3 expression analysis, while ROS levels were assessed using MitoSOX.</div></div><div><h3>Results</h3><div>Silencing OTUD5 significantly reduced lung injury, evidenced by improved histological architecture and decreased collagen deposition. OTUD5 knockdown attenuated apoptosis markers and ROS production in BEAS-2B cells exposed to hyperoxia. Co-IP assays confirmed that OTUD5 stabilizes TRAF4, linking it to the activation of the p38/JNK signaling pathway. Furthermore, treatment with metformin and berberine chloride diminished the protective effects of OTUD5 knockdown in vivo.</div></div><div><h3>Conclusion</h3><div>OTUD5 plays a critical role in hyperoxia-induced lung injury through the regulation of TRAF4 stability and apoptotic pathways. Targeting OTUD5 may provide a novel therapeutic strategy to mitigate lung damage in conditions characterized by oxidative stress.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 103008"},"PeriodicalIF":2.7,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144270713","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":"Impact of mild prenatal LPS-induced inflammation and postnatal stress on synaptic plasticity and neuroimmune responses in the prefrontal cortex of adult male mice","authors":"Zahra Namvarpour ,&nbsp;Sara Azhdari ,&nbsp;Reza Lotfi ,&nbsp;Hasan Pahang ,&nbsp;Hamidreza Omidi ,&nbsp;Mozhdeh Namvarpour ,&nbsp;Abdollah Amini","doi":"10.1016/j.tice.2025.103007","DOIUrl":"10.1016/j.tice.2025.103007","url":null,"abstract":"<div><div>Mild maternal immune activation (MIA) alone has been reported to exert minimal effects on the newborn brain, but when combined with postnatal stress (PS), it can trigger significant and, lasting neuro developmental changes. This study investigated the effects of MIA, alone and in combination with PS, on synaptic plasticity and molecular pathways in the prefrontal cortex, with a focus on potential links to neurodevelopmental disorders. Pregnant mice received an intraperitoneal injection of lipopolysaccharide (LPS, 50 μg/kg) or sterile normal saline on gestational day 17 (GD17). Offspring were exposed to prepubertal stress or no stress from postnatal days 30–38. Two male pups per litter (totally n = 6/ per group) were randomly selected at postnatal day 56 day for prefrontal cortex analysis. Histological, structural, and molecular analyses were conducted, including immunohistochemistry and gene expression analysis. The LPS+Stress group revealed a significant (<em>P &lt; 0.05</em>) reduction in astrocyte-related synaptic cells compared with the LPS, stress control groups. Expression levels of synaptic plasticity-related proteins and genes (BDNF, GAP-43, N-cadherin, synapsin-1, and GFAP) were significantly (<em>P &lt; 0.05</em>) reduced in the LPS+Stress group compared to all other groups. While MIA and PS independently induced subtle synaptic and inflammatory changes, their combined effects were significantly amplified, leading to aberrant molecular expression critical for synaptic function. These findings suggest that the combined effects of mild MIA and PS may exacerbate synaptic and inflammatory dysregulation, potentially increasing susceptibility to neurodevelopmental disorders. Future research should explore potential therapeutic strategies to mitigate the synergistic effects of MIA and PS on neurodevelopment.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 103007"},"PeriodicalIF":2.7,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144222738","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":"Testicular injuries from 45 min of renal ischemia after 24 and 48 h of reperfusion","authors":"Gholampour Firouzeh ,&nbsp;Shojaeddin Badralsadat ,&nbsp;Monsefi Malihezaman ,&nbsp;Karimi Zeinab","doi":"10.1016/j.tice.2025.103006","DOIUrl":"10.1016/j.tice.2025.103006","url":null,"abstract":"<div><div>Ischemia/reperfusion (I/R)-induced acute renal failure (ARF) is linked to oxidative stress and inflammation, which can adversely affect other organs. The degree of injury and subsequent recovery in these organs is determined by the expression of specific molecules during reperfusion, as well as the ischemia's severity and duration. This study investigated how varying durations of reperfusion impact testicular function and sperm characteristics, including count and morphology, after ischemic acute renal failure in male rats. Male Sprague-Dawley rats (n = 7 per group) were divided into three groups: a sham group without renal artery occlusion and two ischemia/reperfusion (I/R) groups subjected to 45 min of bilateral, followed by reperfusion for either 24 h (I/R-24h) or 48 h (I/R-48h). Blood samples were analyzed for plasma levels of creatinine, blood urea nitrogen, testosterone, luteinizing hormone, and follicle-stimulating hormone. Following deep anesthesia, the left testis and kidney were excised for histopathological evaluation and malondialdehyde level measurement. Results showed that 24 h of reperfusion after 45 min of ischemia elevated plasma creatinine and BUN levels, decreased testosterone, and increased levels of inflammatory markers (TLR4, NFĸB, TNF-α) in testis tissue. However, sperm count and morphology remained unchanged. Extending the reperfusion to 48 h mitigated these effects, suggesting that prolonged reperfusion reduces oxidative stress and inflammation, thereby alleviating testicular damage.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 103006"},"PeriodicalIF":2.7,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144230865","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":"Syringetin ameliorates thallium sulphate induced renal dysfunction via regulating Nrf2/Keap-1, TLR4/HMGB1/RAGE and NF-κB pathway","authors":"Hassan M. Otifi ,&nbsp;Muhammad Faisal Hayat ,&nbsp;Ali Akbar ,&nbsp;Syeda Sania Zahara ,&nbsp;Khalid J. Alzahrani ,&nbsp;Fuad M. Alzahrani ,&nbsp;Khalaf F. Alsharif","doi":"10.1016/j.tice.2025.103003","DOIUrl":"10.1016/j.tice.2025.103003","url":null,"abstract":"<div><div>Thallium sulphate (TLM) is a highly hazardous metal known to induce severe renal damage. Syringetin (SGN) is a naturally derived polyphenolic compound that demonstrates excellent medicinal properties. This research trial was conducted to determine the nephroprotective ability of SGN to inhibit TLM induced renal toxicity in rats by assessing different parameters including oxidative stress, apoptotic and inflammatory markers as well as histo-morphological parameters. Thirty-two Sprague Dawley rats were apportioned into the control, TLM (6.4 mgkg⁻¹), TLM (6.4 mgkg⁻¹) + SGN (10 mgkg⁻¹) and SGN (10 mgkg⁻¹) alone administered group. Our findings revealed that TLM exposure promoted renal inflammation which was evident by increased mRNA expression of <em>myeloid differentiation primary response 88 (MYD88), toll-like receptor 4 (TLR4), interleukin-1β</em> (IL-1β), <em>high mobility group box1 (HMGB1), tumor necrosis factor- α (TNF-α), receptor for advanced glycation end products (RAGE), cyclooxygenase-2 (COX-2)</em>, <em>interleukin-6 (IL-6), and nuclear factor- kappa B (NF-κB).</em> The concentrations of reactive oxygen species (ROS) and malondialdehyde (MDA) were exacerbated while the enzymatic action of heme oxygenase-1 (HO-1), superoxide dismutase (SOD), glutathione reductase (GSR), catalase (CAT), &amp; tissue contents of glutathione (GSH) were reduced after TLM intoxication. Serum concentrations of N-Acetylglucosamine (NAG), blood urea nitrogen (BUN), Kidney Injury Molecule-1 (KIM-1), Neutrophil Gelatinase-Associated Lipocalin (NGAL), creatinine, uric acid were observed elevated while a notable reduction was noted in the concentration of creatinine clearance following the dose administration of TLM. The levels of Bcl-2–associated X protein (Bax), cysteine-aspartic acid protease-3 (Caspase-3) &amp; cysteine-aspartic acid protease-9 (Caspase-9) were exacerbated while the concentration of B-cell lymphoma-2 (Bcl-2) was notably suppressed following regimen of TLM. Renal tissues were distorted after TLM administration. In contrast, SGN supplementation notably restored oxidative profile, reduced pro-inflammatory and apoptotic markers as well as improved renal histology.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 103003"},"PeriodicalIF":2.7,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144241038","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":"Pinobanksin ameliorates perfluorooctane sulfonate-evoked cardiotoxicity via targeting Nrf-2/Keap-1, oxidative damage and inflammation in Sprague Dawley rats","authors":"Maryam Javed ,&nbsp;Quratulann Sattar ,&nbsp;Muhammad Faisal Hayat ,&nbsp;Hamida Hamdi ,&nbsp;Muhammad Zaid Salar","doi":"10.1016/j.tice.2025.102988","DOIUrl":"10.1016/j.tice.2025.102988","url":null,"abstract":"<div><div>Perfluorooctane sulfonate (PFOS) is a potent environmental toxicant which affects crucial organs of the body including the heart. Pinobanksin (PBN) exhibits marvelous medicinal values owing to its excellent therapeutic properties. This investigation was executed to assess the curative potential of PBN against PFOS instigated cardiac dysfunction in rats. Twenty-four albino rats (<em>Rattus norvegicus</em>) were apportioned into 4 groups including the control, PFOS (10 mgkg^-1), PFOS (10 mgkg^-1) + PBN (20 mgkg^-1) and PBN (20 mgkg^-1) alone provided group. Our findings showed that PFOS intoxication reduced the activities of glutathione reductase (GSR), superoxide dismutase (SOD), glutathione peroxides (GPx), glutathione S-transferase (GST), Heme Oxygenase-1 (HO-1) and catalase (CAT) while reducing the concentrations of malondialdehyde (MDA) and reactive oxygen species (ROS). Moreover, PFOS intoxication increased the concentrations of creatine kinase-myocardial band (CK-MB), creatine phospho-kinase (CPK), lactate dehydrogenase (LDH) and troponin I. Furthermore, cardiac inflammation was provoked after PFOS provision that was evident by augmented levels of pro-inflammatory markers. The administration of PFOS upregulated the expressions of Bcl-2–associated X protein (Bax) and cysteine-aspartic acid protease-3 (caspase-3), while reducing the expressions of B-cell lymphoma protein 2 (Bcl-2). Nonetheless, the histopathological analysis showed significant cardiac damage after PFOS intoxication. However, PBN treatment alleviated cardiac impairments because of its tremendous oxidation curtailing properties.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 102988"},"PeriodicalIF":2.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144262639","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}