Tissue & cell最新文献

{"title":"Dual actions of apelin-13 in TNBS-induced colitis: Colonic protection via the gut–liver axis but intrinsic hepatotoxic potential following systemic administration","authors":"Ilknur Birsen ,&nbsp;Kamil Erdogan ,&nbsp;Ozlem Ozsoy ,&nbsp;Sevil Aksu ,&nbsp;Ozlem Ozbey Unlu ,&nbsp;Gizem Korkmaz ,&nbsp;Vecihe Nimet Izgut-Uysal","doi":"10.1016/j.tice.2025.103276","DOIUrl":"10.1016/j.tice.2025.103276","url":null,"abstract":"<div><div>Inflammatory bowel disease (IBD) is a systemic condition that can also lead to extraintestinal complications, including liver damage. Disruptions in the gut–liver axis and inflammatory mediators play a key role in this process. Apelin, a peptide involved in inflammation, oxidative stress, and apoptosis, has shown protective effects in the colon during IBD; however, its hepatic actions remain unclear, making it crucial to clarify its systemic impact on the gut–liver axis.</div><div>This study aimed to evaluate the effects of apelin-13 on liver injury associated with colitis using a trinitrobenzene sulfonic acid (TNBS)-induced colitis model. Wistar rats were divided into five groups (n = 8 per group): normal control (NC), ethanol control (EC), apelin (AP), colitis (TNB), and colitis + apelin (TNB+AP). Colitis was induced via intrarectal administration of TNBS (100 mg/kg in 50 % ethanol), and apelin-13 (150 µg/kg/day, i.p.) was administered for three days following induction.</div><div>Apelin-13 reduced colitis severity, by reducing weight loss, colon damage, and disease activity index (DAI), and improved intestinal barrier integrity by increasing zonula occludens-1 (ZO-1) expression, thereby reducing portal tumor necrosis factor (TNF-α) and lipopolysaccharide (LPS) levels. However, apelin-13 did not prevent TNBS-induced hepatic inflammation or oxidative stress and, when administered alone, caused mild hepatocellular injury, with increased necrosis, TNF-α, malondialdehyde (MDA), and alanine aminotransferase (ALT) levels.</div><div>In conclusion, apelin-13 ameliorates colitis and modulates gut–liver axis signaling but fails to confer hepatic protection. This outcome suggests that gut-mediated benefits may be offset by mild hepatic stress caused by systemic apelin exposure, resulting in a neutral overall liver response. These findings emphasize that apelin-based interventions in IBD may require targeted delivery strategies to retain intestinal benefits while minimizing hepatic exposure.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103276"},"PeriodicalIF":2.5,"publicationDate":"2025-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145775928","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":"Mast cell characterization, density, and distribution in placenta accreta spectrum: A histological, histochemical and immunohistochemical analysis","authors":"Thaer Bahjat ,&nbsp;Malak AL-Yawer ,&nbsp;Haydar Al- Shamaa","doi":"10.1016/j.tice.2025.103273","DOIUrl":"10.1016/j.tice.2025.103273","url":null,"abstract":"<div><div>The placenta accreta spectrum (PAS) is a group of disorders characterized by abnormal trophoblastic invasion, often associated with decidual defects, stromal remodeling, and immune dysregulation, resulting in serious obstetric complications. Mast cells (MCs), known for their roles in tissue remodeling, angiogenesis, and inflammation, have not been fully explored in the context of PAS. This study aimed to investigate the morphological, phenotypic, and quantitative alterations of MCs in PAS compared to normal placentas using a multimodal histopathological approach. Placental tissues from PAS cases and gestational age-matched controls were examined using hematoxylin and eosin (H&amp;E), toluidine blue (TB), Alcian blue/safranin (A/S), and immunohistochemistry (IHC) with anti-tryptase antibodies. MC density, distribution, morphology, and activation status were assessed in the decidual, villous, and myometrial compartments and statistical comparisons were made using t-tests and two-way ANOVA. The results showed a significant increase in MC density in PAS placentas across all staining methods (p &lt; 0.05). Histochemical stains revealed a greater number of morphologically activated MCs, particularly connective tissue-type mast cells (CTMCs), in PAS tissues. IHC confirmed elevated counts of tryptase-positive MCs exhibiting features of degranulation, especially in areas adjacent to trophoblastic invasion and stromal disruption. Statistical analysis indicated a significant effect of both diagnosis and staining technique on MC counts (p &lt; 0.001). These findings suggest that MCs are increased and activated in PAS, with potential roles in extracellular matrix (ECM) degradation, inflammation, and abnormal implantation. The predominance of CTMCs and their spatial association with invasive extravillous trophoblasts point to a contributory role in PAS pathophysiology. Further research using expanded immunomarker panels, functional assays, and more diverse study populations is needed to determine whether MCs are causal agents or secondary responders in PAS and to assess their potential as diagnostic or therapeutic targets.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103273"},"PeriodicalIF":2.5,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145794910","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":"Membrane-engineered Wharton’s Jelly derived mesenchymal stem cells with anti-CD2 antibody coating modulate activated CD3+ T-cell responses","authors":"Hilal Özçelik ,&nbsp;Yusufhan Yazır ,&nbsp;Gökhan Duruksu ,&nbsp;Kamil Can Kılıç ,&nbsp;Ahmet Öztürk","doi":"10.1016/j.tice.2025.103274","DOIUrl":"10.1016/j.tice.2025.103274","url":null,"abstract":"<div><h3>Objective</h3><div>Mesenchymal stem cells (MSCs) regulate immunity through paracrine signaling and direct interactions by secreting cytokines and biological factors, yet effective therapy requires large numbers of MSCs. This study aimed to improve the interaction between human Wharton’s Jelly-derived mesenchymal stem cells (hWJ-MSCs) and activated CD2⁺/CD3⁺ T lymphocytes by incorporating anti-CD2 antibodies into their cell membranes. This strategy was grounded in the recognition that MSC immunoregulatory efficacy depends on both soluble mediators and receptor-mediated cell-cell contact, and that strengthening this interface enhances their functional engagement with activated T-cells.</div></div><div><h3>Methods</h3><div>In this study, hWJ-MSCs were coated with a palmitic acid-conjugated protein G (PPG) system to anchor anti-CD2 antibodies onto the cell membrane. Cytocompatibility of coating was evaluated using WST-8 assay, and 20 µg/mL was identified as optimal concentration. After coating and T-cell isolation, a 48-hour co-culture was established with phytohemagglutinin (PHA)-stimulated CD2⁺/CD3⁺ T lymphocytes and β-cells. Cellular responses were evaluated using WST-8, Live/Dead staining, CFSE proliferation assay, DCFDA-based ROS analysis, and CD3 flow cytometry to assess viability, proliferation, and oxidative activity of PBMCs. β-cell function was assessed by measuring insulin secretion using a single ELISA assay as a functional outcome indicator, without further mechanistic analysis.</div></div><div><h3>Results</h3><div>The WST-8 assay demonstrated that 20 µg/mL PPG maintained approximately 80 % cell viability, and this concentration was selected as the optimal dose for subsequent experiments. Anti-CD2 and anti-PPG antibodies were purified using the FPLC method. CD25 and CD2 marker expression increased following PHA stimulation. CFSE staining showed higher fluorescence intensity in the MSC-coated group than in the non-coated group, indicating suppressed T-cell proliferation. DCFDA staining revealed reduced ROS levels in the coated group, while the WST-8 test indicated lower viability in MSC-coated groups relative to controls. ELISA analysis showed the highest insulin secretion in the MSC-coated group.</div></div><div><h3>Conclusion</h3><div>Anti-CD2 antibody-conjugated PPG-coated hWJ-MSCs reduced T-cell viability, proliferation, and WST-8-based metabolic activity while also attenuating DCFDA-detected ROS compared with uncoated cells. ROS levels remained elevated in CD2-only group. Coated MSCs therefore produced a more controlled and less inflammatory T-cell response within co-culture system. These findings suggest that surface-engineered hWJ-MSCs may enhance immunoregulatory performance of MSC-based approaches for T-cell-mediated autoimmune disorders, including Type 1 Diabetes Mellitus (T1DM).</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103274"},"PeriodicalIF":2.5,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145744744","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":"Niaodukang for the treatment of chronic kidney disease: Regulation of the TRAF3/NF-κB2 signaling pathway and its improvement of the intestinal barrier","authors":"Juan Xu ,&nbsp;Lei Wang ,&nbsp;Hong Wang ,&nbsp;Jie Pang ,&nbsp;Linna Liu ,&nbsp;Ting Zhang ,&nbsp;Ling Yuan ,&nbsp;Xiaoxue Cui ,&nbsp;Qian Jiang ,&nbsp;Yanlin Li","doi":"10.1016/j.tice.2025.103271","DOIUrl":"10.1016/j.tice.2025.103271","url":null,"abstract":"<div><h3>Background</h3><div>Niaodukang (NDK) mixture is a traditional Chinese herbal formula clinically used for chronic kidney disease (CKD). However, its bioactive components and molecular mechanisms remain unclear.</div></div><div><h3>Objective</h3><div>To explore the protective effect of NDK on CKD-associated intestinal barrier dysfunction and identify its key active compound targeting the TRAF3/NF-κB2 pathway.</div></div><div><h3>Methods</h3><div>A 5/6 nephrectomy rat model and indole-induced Caco-2 cell injury model were established. Renal function, intestinal tight junction integrity, and inflammatory signaling were evaluated by histological, molecular, and ultrastructural analyses. Network pharmacology and molecular docking were applied to predict bioactive compounds, followed by in vitro validation.</div></div><div><h3>Results</h3><div>NDK significantly improved renal function (reduced Scr, BUN, and urine protein; <em>P</em> &lt; 0.01) and restored intestinal epithelial barrier integrity, as indicated by increased ZO-1 and occludin expression and improved ultrastructure. Among 126 candidate compounds, formononetin from Astragalus membranaceus exhibited strong binding affinity to TRAF3. Functional assays confirmed that formononetin suppressed TRAF3/NF-κB2 signaling, restored tight junction proteins, and alleviated epithelial injury, whereas TRAF3 overexpression abolished these protective effects.</div></div><div><h3>Conclusion</h3><div>NDK ameliorates CKD-associated intestinal barrier dysfunction by suppressing the TRAF3/NF-κB2 pathway. Formononetin serves as a principal active compound mediating this effect, elucidating the pharmacological basis of NDK and supporting its therapeutic potential for CKD.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103271"},"PeriodicalIF":2.5,"publicationDate":"2025-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145769233","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":"Black tea extract exerts a protective effect on diethylnitrosamine-induced hepatic precancerous lesions through the Nrf2 signaling pathway","authors":"Xiu Wang ,&nbsp;Ying-hao Hu ,&nbsp;Jia-jia Luo,&nbsp;Yan Wang","doi":"10.1016/j.tice.2025.103260","DOIUrl":"10.1016/j.tice.2025.103260","url":null,"abstract":"<div><h3>Objective</h3><div>To investigate the protective effect and mechanism of black tea (BT) extract on diethylnitrosamine (DEN)-induced liver precancerous lesions in rats.</div></div><div><h3>Methods</h3><div>Fifty male Sprague-Dawley (SD) rats were randomly assigned to five groups: normal control, DEN model, and three black tea extract groups (low, medium, and high dose: DEN+BT-L, DEN+BT-M, DEN+BT-H). The model and treatment groups received DEN (50 mg/kg, i.p.) for 14 weeks, and black tea extract (25, 50, or 100 mg/kg) was administered via gavage. Liver histopathology was evaluated by hematoxylin-eosin (HE) and Masson staining. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), alpha-fetoprotein (AFP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were assessed. Hepatic oxidative stress markers—reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA)—were measured. Expression of nuclear factor erythroid 2–related factor 2 (Nrf2), heme oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3 (p-STAT3), nuclear factor-kappa B (p65), and phosphorylated p65 (p-p65) was evaluated by Western blot.</div></div><div><h3>Results</h3><div>Black tea extract alleviated DEN-induced hepatocyte damage, fibrosis, and inflammation. It reduced serum ALT, AST, ALP, AFP, IL-6, and TNF-α levels, decreased ROS and MDA, and increased SOD and GSH levels in a dose-dependent manner (P &lt; 0.05). Nrf2 and HO-1 protein levels were upregulated, while STAT3, p-STAT3, p65, and p-p65 expressions were downregulated. NQO1 expression showed a decreasing trend.</div></div><div><h3>Conclusions</h3><div>Black tea extract protects against DEN-induced liver precancerous changes by enhancing antioxidant capacity via the Nrf2/HO-1 pathway and inhibiting the NF-κB/STAT3 axis, suggesting its potential in preventing liver carcinogenesis.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103260"},"PeriodicalIF":2.5,"publicationDate":"2025-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145821101","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":"INHBB promotes liver metastasis of colorectal cancer via regulation of TGF-β/Smad signaling, EMT and anoikis resistance","authors":"Nianzhao Yang ,&nbsp;Dafei Dai ,&nbsp;Jun Zhao ,&nbsp;Haiyuan Zhao ,&nbsp;Haibo Jiang ,&nbsp;Jun Liu ,&nbsp;Fubao Liu ,&nbsp;Xiaopeng Chen","doi":"10.1016/j.tice.2025.103258","DOIUrl":"10.1016/j.tice.2025.103258","url":null,"abstract":"<div><h3>Background</h3><div>Colorectal cancer (CRC) is the third most prevalent malignancy worldwide, with liver metastasis being a major cause of mortality. Although Inhibin β B (INHBB) is associated with tumor progression, its specific role in CRC liver metastasis remains poorly understood.</div></div><div><h3>Methods</h3><div>Transcriptomic analysis of GEO/TCGA datasets identified INHBB as a key regulator of anoikis resistance and liver metastasis in colorectal cancer. Comprehensive bioinformatics analyses were performed, including clinicopathological correlation assessment, prognostic evaluation, immune landscape characterization, drug sensitivity prediction, and functional enrichment studies. Functional validation included: (1) molecular profiling (qPCR/Western blot/IHC), (2) siRNA-mediated knockdown in HCT116/Caco-2 cells with functional assays (transwell migration/invasion, calcein AM/EthD-1 anoikis detection), and (3) mechanistic interrogation of TGF-β/Smad signaling, EMT markers, and anoikis-related proteins. In vivo validation was performed using a mouse model with spleen injection.</div></div><div><h3>Results</h3><div>Our study systematically characterized the expression profile of INHBB in primary CRC and liver metastases, revealing significantly elevated expression in both tissue types (P &lt; 0.01). Clinicopathological analysis demonstrated that high INHBB expression correlated significantly with advanced TNM stage (III-IV), lymph node metastasis (N1–2), and poor prognosis (P &lt; 0.001). Functionally, INHBB knockdown reduced CRC cell migration, invasion, and hepatic metastasis formation (all P &lt; 0.01) through three distinct mechanisms: (1) attenuating TGF-β/Smad2/3/Smad4 signaling (evidenced by decreased Smad2/3 phosphorylation, P &lt; 0.01), (2) reversing EMT progression (E-cadherin upregulation concomitant with N-cadherin and vimentin downregulation), and (3) sensitizing cells to anoikis (INHBB interference significantly increased the anoikis rate). Immune profiling revealed that INHBB positively correlated with M0/M1 macrophages and resting NK cells (P &lt; 0.05), but negatively with resting dendritic cells, mast cells, eosinophils, and plasma cells (P &lt; 0.05), suggesting its potential role in remodeling the immune microenvironment to facilitate tumor immune escape. Our in vivo studies demonstrated that INHBB silencing significantly inhibited colorectal cancer liver metastasis in a xenograft mouse model.</div></div><div><h3>Conclusion</h3><div>Our study demonstrates that INHBB drives CRC liver metastasis by upregulating the TGF-β/Smad2/3/Smad4 pathway and anoikis resistance, highlighting its potential as a therapeutic target and prognostic biomarker for metastatic CRC.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103258"},"PeriodicalIF":2.5,"publicationDate":"2025-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145744738","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":"Quercetin targeted NF-κB to regulate platelet activation and prevent arterial thrombosis","authors":"Wenli Wang ,&nbsp;Yanmei Li ,&nbsp;Yanyan Liu ,&nbsp;Zhangping Sun ,&nbsp;Bingiie Zhao ,&nbsp;Fubo Song","doi":"10.1016/j.tice.2025.103270","DOIUrl":"10.1016/j.tice.2025.103270","url":null,"abstract":"<div><div>While the inactivation effect of quercetin on platelets has been widely studied, the underlying mechanisms remained insufficiently explored. This research examined how quercetin inactivated platelets and helps to prevent thrombosis. We validated quercetin's inhibitory effects on platelet activation by CRP and collagen. We also investigated how quercetin regulated the NF-κB pathway during platelet activation and its potential impact on this process. To validate <em>in vitro</em> results, we created an <em>in vivo</em> arterial thrombus model using FeCl₃ and observed thrombus formation after quercetin administration. Quercetin inhibited platelet activation by CRP and collagen, reduced aggregation rate, and suppressed adhesion to collagen surface. This effect was linked to the NF-κB pathway. The <em>in vitro</em> results were validated in a FeCl₃-induced carotid artery thrombosis model. The effects of quercetin, as previously mentioned, were observed to be dose-dependent. Furthermore, the essential function of the NF-κB signaling pathway in this process has been substantiated. NF-κB was the drug target of quercetin. However, the inhibitory effect of quercetin was attenuated when the NF-κB pathway was pre-activated. Our study confirmed the antiplatelet and antithrombotic effects of quercetin. This study not only confirmed that quercetin exerted its antithrombotic effects by inhibiting the NF-κB pathway but also, more importantly, clearly identified NF-κB p65 as a direct target of quercetin through molecular docking and DARTS assays.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103270"},"PeriodicalIF":2.5,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145744696","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":"U0126 induces osteoclast differentiation via the p38-NFATc-1 signaling pathway","authors":"Jiran Wang ,&nbsp;Jinan Liu ,&nbsp;Xueting Jia ,&nbsp;Guangyong Chen ,&nbsp;Shuzhen Chen ,&nbsp;Xiaofeng Huang","doi":"10.1016/j.tice.2025.103263","DOIUrl":"10.1016/j.tice.2025.103263","url":null,"abstract":"<div><div>Osteoclast differentiation plays an important role in bone metabolic diseases, such as osteoporosis, osteosclerosis and so on. In the study, we found that the ERK inhibitor, U0126, significantly increased the number of multinucleated osteoclasts after inducing differentiation of mouse mononuclear macrophage RAW264.7 cells. The Shh-p38-NFATc-1 signaling pathway has been reported to induce osteoclast differentiation in our previous work, and here U0126 also could increase pp38 and NFATc-1 expression as well as NFATc-1 entrance into the nucleus. Animal experiment demonstrated that U0126 accelerated tooth eruption in newborn mice and promoted alveolar bone resorption by inducing osteoclastogenesis. Furthermore, U0126 can rescue delayed tooth eruption caused by LDE225 (a Shh inhibitor) suppression of the p38 signaling pathway. Cytological experiments also revealed that U0126 could rescue the osteoclastic inhibitory effect of LDE225, but not Doramapimod (a p38 inhibitor). Therefore, we conclude that U0126 promotes osteoclast differentiation via the p38-NFATc-1 signaling pathway and relieves the inhibitory effect of LDE225 on osteoclastogenesis. Our study may provide a scientific foundation for dental treatment strategies to enhance osteoclast function in addressing tooth eruption issues, such as impacted teeth, delayed eruption of permanent teeth, and cranioclavicular dysplasia syndrome (CCD). It will also serve as a method for future research into novel approaches to treating disorders linked to bone metabolism.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103263"},"PeriodicalIF":2.5,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145715934","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":"Ultrastructural configuration of porcine liver preserved by machine perfusion versus static cold storage donated cardiac after death","authors":"Hiroki Bochimoto ,&nbsp;Nur Khatijah Mohd Zin ,&nbsp;Yo Ishihara ,&nbsp;Tetsuya Nakajo ,&nbsp;Hiromichi Obara ,&nbsp;Naoto Matsuno ,&nbsp;Daisuke Kondoh","doi":"10.1016/j.tice.2025.103262","DOIUrl":"10.1016/j.tice.2025.103262","url":null,"abstract":"<div><div>In liver transplantation, it is known that machine perfusion (MP) preservation of liver grafts donated after cardiac death is superior to static cold storage (SCS). However, hepatocyte ultrastructure appears to be normal after SCS, while MP induces significant ultrastructural changes of hepatocytes such as mitochondrial swelling. The differences between these ultrastructural findings and physiological/clinical findings should be evaluated in detail. Here, we examined porcine liver grafts after SCS 4°C or MP at 8°C by osmium-maceration scanning (OM-SEM) and transmission (TEM) electron microscopic analyses. The overall appearance of hepatocytes in the SCS group was relatively normal, while the cytoplasm in the MP group was abnormal with swollen mitochondria and heavily-foamy endoplasmic reticulum. However, bile canaliculi of the liver grafts after SCS were filled with disintegrated materials which represent the exfoliated microvilli, while those after MP had a normal microvilli structure. Liver sinusoidal endothelial cells (LSECs) after SCS showed a heavy cytopathic change accompanied by large vacuoles, whereas LSECs after MP had no or significantly smaller vacuoles that appeared to be autophagosomes. These findings indicated that functional ultrastructure of liver grafts was better preserved in MP condition than in SCS. This is contrary to the impression given by the overall image of hepatocytes, and thus ultrastructural evaluation focusing on specific functional structures like bile canaliculi and LSECs have advantages to of liver grafts. (222/250 words)</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103262"},"PeriodicalIF":2.5,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145796597","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":"Artocarpin alleviates fenofibrate-induced hepatic dysfunction via regulating NLRP3/caspase-1, oxidative stress and bile acids synthesis: A biochemical, histological, and computational investigation","authors":"Mohammed S. Alshammari ,&nbsp;Salim Jamil ,&nbsp;Hafsa Ashfaq ,&nbsp;Ahmed Al-Emam ,&nbsp;Hesham M. Hassan","doi":"10.1016/j.tice.2025.103261","DOIUrl":"10.1016/j.tice.2025.103261","url":null,"abstract":"<div><div>Fenofibrate (FBR) is a promising hypolipidemic drug that is reported to induce hepatic impairments. Artocarpin (ACP) is a novel polyphenolic compound with diverse biological properties. This investigation was planned to explore the palliative efficacy of ACP in combating FBR-induced hepatotoxicity. Thirty-two Sprague Dawley rats were grouped into control, FBR (100 mg/kg), FBR (100 mg/kg) + ACP (100 mg/kg), and ACP (100 mg/kg) alone administered group. Our findings showed that FBR intoxication upregulated the mRNA expressions of CXCR4, CCR5, Caspase-1, IL-1β, CCL2, IL-18 and NLRP3. The levels of ROS and MDA were augmented while the enzymatic action of GST, HO-1, SOD, GPx, GSR, GST, and CAT were suppressed following the exposure of FBR. Besides, FBR intoxication induced cholestatic stress as evidenced by elevated levels of chenodeoxycholic, deoxycholic acid, cholic acid, glycocholic acid and taurocholic acid. The levels of ALP, GGT, AST, hepcidin, and ALT were aggravated while the levels of total protein, hemojuvelin, and albumin were inhibited by FBR administration. Moreover, FBR exposure compromised the morphology of liver by altering key structural components. Importantly, concurrent therapy of ACP restored hepatic health by inhibiting the activation of NLRP3/Caspase-1 pathway, reducing hepatic enzymes, oxidative stress while regulating iron metabolism as well as bile acid metabolic alterations. Furthermore, ACP reversed histological alterations in hepatic tissues. These findings are supported by our in-silico analysis which exhibits excellent modulatory activity of ACP by binding at key regulatory binding sites. Collectively, these results underscore the hepatoprotective efficacy of ACP against FBR-induced liver impairments.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103261"},"PeriodicalIF":2.5,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145747392","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}