Tissue & cell最新文献

{"title":"Resveratrol protects against letrozole-induced renal damage in a rat model of polycystic ovary syndrome: A biochemical, histological, and immunohistochemical study","authors":"Einas M. Yousef ,&nbsp;Samar M. Abd El-moneam ,&nbsp;Shimaa Mohammad Yousof ,&nbsp;Safaa Abdallah Mohammed ,&nbsp;Basma Osman Sultan ,&nbsp;Basma S.A. Mansour","doi":"10.1016/j.tice.2025.102934","DOIUrl":"10.1016/j.tice.2025.102934","url":null,"abstract":"<div><h3>Background</h3><div>Polycystic ovary syndrome (PCOS) is a common endocrine disorder that affects 9–18 % of women, often associated with metabolic and renal complications. This study aimed to investigate the renoprotective effects of resveratrol (RSV) in a letrozole-induced rat model of PCOS, focusing on biochemical, histological, ultrastructural, and immunohistochemical alterations.</div></div><div><h3>Methods</h3><div>Thirty female rats were randomly divided into five groups: negative control, only RSV-treated, PCOS-induced (sham), metformin-treated, and RSV-treated. Serum testosterone, urea, and creatinine levels were assessed. Renal tissues underwent histological, immunohistochemical, ultrastructural, and morphometric analyses. Additionally, TGF-β1 mRNA expression was evaluated using qRT-PCR.</div></div><div><h3>Results</h3><div>Letrozole administration significantly elevated serum testosterone, urea, and creatinine levels, indicating PCOS-associated renal dysfunction. Histological and ultrastructural analysis revealed severe glomerular and tubular alterations in the sham group. The administration of RSV significantly restored renal architecture and function more effectively than metformin. Immunohistochemistry analysis showed that RSV reduced Proliferating Cell Nuclear Antigen (PCNA) overexpression and restored B-cell Lymphoma 2 (BCL-2) expression, suggesting a protective effect against cellular stress and apoptosis. Moreover, RSV significantly downregulated TGF-β1 expression, indicating its anti-fibrotic and anti-inflammatory role in PCOS-related renal damage.</div></div><div><h3>Conclusion</h3><div>In a PCOS rat model, RSV protects effectively against letrozole-induced structural and functional renal damage. It demonstrates superior efficacy over metformin in restoring renal function, reducing apoptosis, and mitigating fibrosis. These findings suggest that RSV may serve as a potential adjunct therapy for preventing PCOS-associated renal complications, emphasizing the need for further investigations.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102934"},"PeriodicalIF":2.7,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890682","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":"Modulation of TLR4 mediated HMGB1/RAGE/NF-κB axis through linarin against fenvalerate provoked cardiotoxicity","authors":"Fuad M. Alzahrani ,&nbsp;Arifa Mehreen ,&nbsp;Qurat Ul Ain ,&nbsp;Adnan Ali ,&nbsp;Khalid J. Alzahrani ,&nbsp;Khalaf F. Alsharif","doi":"10.1016/j.tice.2025.102931","DOIUrl":"10.1016/j.tice.2025.102931","url":null,"abstract":"<div><div>Fenvalerate (FVN) is a potent insecticidal agent that exhibits a wide range of organ impairments including cardiac damage. Linarin (LIN) is a polyphenolic compound with a diverse range of pharmacological potentials. The present investigation was conducted to quantify the mitigative ability of LIN against FVN induced cardiotoxicity. Thirty-six male Sprague Dawley rats were divided into four groups i.e., the control, FVN (40 mg/kg), FVN (40 mg/kg) + LIN (50 mg/kg) and LIN (50 mg/kg) alone treated group. It was observed that FVN exposure exacerbated the gene expression of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), receptor for advanced glycation end products (RAGE), interleukin-1β (IL-1β), high mobility group box 1 (HMGB1), cyclooxygenase-2 (COX-2), nuclear factor- kappa B (NF-κB), toll-like receptor 4 (TLR4), and tumor necrosis factor-α (TNF-α). Moreover, the levels of reactive oxygen species (ROS) &amp; malondialdehyde (MDA) were surged-up while the enzymatic action of heme oxygenase-1 (HO-1), glutathione (GSH), glutathione Peroxidase (GPx), superoxide dismutase (SOD), glutathione reductase (GSR), and catalase (CAT) were decreased following the FVN intoxication. Besides, FVN administration upregulated the concentrations of troponin-I, troponin-T, c-reactive protein, creatine kinase-MB (CK-MB), creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) in cardiac tissues. FVN exposure increased the levels of Caspase-9, Bax and Caspase-3 while reducing the levels of Bcl-2. Cardiac tissues showed abnormal morphology after FVN intoxication. Nonetheless, LIN therapy remarkably alleviated cardiac damages instigated through FVN exposure due to its anti-inflammatory, anti-oxidative as well as anti-apoptotic potentials.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102931"},"PeriodicalIF":2.7,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890557","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":"Mechanism of the effect of Juan-Tong-Yin on endoplasmic reticulum stress-autophagy in endometriosis rats based on protein kinase R-like endoplasmic reticulum kinase/eukaryotic cell initiation factor 2α pathway","authors":"Qi-Yu Liu ,&nbsp;Jing Li ,&nbsp;Feng-Qun Gu ,&nbsp;Feng-Yun Meng ,&nbsp;Ying Liu ,&nbsp;Wei-Hong Li","doi":"10.1016/j.tice.2025.102935","DOIUrl":"10.1016/j.tice.2025.102935","url":null,"abstract":"<div><h3>Objective</h3><div>To explore the mechanism of Juan-Tong-Yin (JTY) on endoplasmic reticulum (ER) stress-autophagy in endometriosis (EM) rats through the protein kinase R-like endoplasmic reticulum kinase (PERK)/eukaryotic cell initiation factor 2α (eIF2α) autophagy pathway.</div></div><div><h3>Methods</h3><div>An EM rat model was established. A total of 70 Sprague–Dawley (SD) rats were randomly divided into the normal control group, model group, JTY high-, medium- and low-dose groups (25.4, 12.7, and 6.35 g/kg, respectively), progesterone group (0.26 mg/kg), and ER stress group (2-DG, 100 mg/kg). The seven groups were given the corresponding dose of the drug through gavage in the administration group and saline through gavage (1 mL/100 g) in the model and normal control groups. The drugs were administered continuously for 4 weeks. Ectopic lesion volume and pelvic adhesion score were measured. Hematoxylin-eosin (HE) staining was used to observe the pathological changes of ectopic endothelium in rats. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of serum inflammatory marker C-reactive protein (CRP) and estradiol (E2) in each group; immunohistochemistry, real-time fluorescence quantitative polymerase chain reaction (Real-time PCR), and protein immunoblotting method (Western blotting) were used to detect the expressions of ectopic endothelial PERK, eIF2α, and microtubule-associated protein light chain 3B (LC3B) and mRNA.</div></div><div><h3>Results</h3><div>Compared with the model group, the JTY-treated rats exhibited significantly reduced ectopic lesion volume (P &lt; 0.05), the pelvic adhesion score was decreased (<em>P</em> &lt; 0.05), and the pathology of the ectopic endothelium showed varying degrees of atrophy, detachment, and gland reduction. In addition, serum inflammatory marker CRP and E2 levels were decreased significantly, and JTY promoted the expression of PERK, eIF2α, and microtubule-associated protein LC3B protein and mRNA (<em>P</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>JTY ameliorates EM by activating the PERK/eIF2a pathway, enhancing cell ER stress and autophagy, improving the inflammatory microenvironment, and ultimately mitigating EM in rats.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102935"},"PeriodicalIF":2.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890556","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":"Ferroptosis targeting offers a therapeutic target for septic cardiomyopathy","authors":"Pengsi Zhou,&nbsp;Mengxue Liu,&nbsp;Tao Lv","doi":"10.1016/j.tice.2025.102930","DOIUrl":"10.1016/j.tice.2025.102930","url":null,"abstract":"<div><div>Sepsis-induced cardiac dysfunction, usually termed sepsis-induced cardiomyopathy or septic cardiomyopathy(SCM), is developed in approximately 70 % of the patients with sepsis, making it is a major concern for sepsis patients. However, the pathogenesis of SCM remain incompletely understood. Ferroptosis, a newly identified mechanism of regulated cell death, characterized by a decline in antioxidant capacity, iron accumulation, and lipid peroxidation(LPO), is involved in sepsis and SCM. Moreover, ferroptosis inhibitors confer a novel therapeutic regimen in SCM. In this Review, we first summarizes the core mechanism of ferroptosis, with an emphasis on how best to interpret ferroptosis leads to the genesis of SCM. We then highlights our focus on the emerging different types of therapeutic ferroptosis inhibitors and summarizes their pharmacological beneficial effect to treat SCM. This review highlights a novel potential therapeutic strategy for SCM by pharmacologically inhibiting ferroptosis.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102930"},"PeriodicalIF":2.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143874831","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":"The protective effect of Ambrosia maritima versus vitamin D3 against gentamicin-induced acute cortical kidney injury in adult male albino rats: Histological and immunohistochemical study","authors":"Eman A. El-Sawaf ,&nbsp;Basma H. Amin ,&nbsp;Mohammed Yosri ,&nbsp;Heba Bayoumi ,&nbsp;Marwa M. Hassan","doi":"10.1016/j.tice.2025.102939","DOIUrl":"10.1016/j.tice.2025.102939","url":null,"abstract":"<div><div>Gentamicin (GM) is a broad-spectrum antibiotic widely used for severe bacterial infections, but it<!--> <!-->is associated with acute nephrotoxicity. <em>Ambrosia maritima</em> L. is an annual herbaceous plant that has a<!--> <!-->variety of medicinal and antioxidant activities. Vitamin D3 is involved in a multitude of biological functions and essential antioxidant pathways. This study aims to investigate the protective effects of Damsissa (<em>Ambrosia maritima</em>) versus vitamin D3 against GM-induced nephrotoxicity using 72 male rats that were randomly divided into six groups: control, Damsissa (100 mg/kg/day), vitamin D3 (1000 IU/kg/day), GM<!--> <!-->(100 mg/kg/day for 7 days), GM + Damsissa, and GM + vitamin D3. Renal function, oxidative stress biomarkers (MDA, CAT, SOD, GSH), cytokine levels (IL-1β, IL-6, TNF-α, IL-4), and gene expression (<em>Caspase-3</em>, <em>Keap1</em>, <em>PPARγ, Nrf2</em>) were assessed. Histopathological and ultrastructural kidney analyses were conducted using H&amp;E, Masson’s trichrome, PCNA staining, and transmission electron microscopy. Blood samples were tested for renal and liver markers (creatinine, BUN, AST, ALT). Damsissa enhanced survival rates, returned the renal indices to near normal, and ameliorated pathological changes based on immunohistopathological and ultrastructural results. They further reduced pro-inflammatory cytokine production, optimized oxidative stress markers, and normalized gene expression levels. Both treatments exhibited abundant antioxidant and anti-inflammatory effects, which remarkably reduced GM-induced acute kidney injury. These results suggest that both Damsissa and vitamin D3 may exert protective effects against drug-induced nephrotoxicity.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102939"},"PeriodicalIF":2.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890681","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":"Enhanced hepatoprotective efficacy of quercetin nanoparticles versus free quercetin against acrylamide-induced hepatotoxicity through modulation of MAPK/NF-κB/NLRP3 signaling pathways and molecular docking validation","authors":"Rasha Atta ,&nbsp;Horeya Erfan Korayem Arafat ,&nbsp;Islam A. Khalil ,&nbsp;Dina A. Ali ,&nbsp;Noha M. Abd El-Fadeal ,&nbsp;Shahad W. Kattan ,&nbsp;Walla Alelwani ,&nbsp;Manal S. Fawzy ,&nbsp;Mona F. Mansour","doi":"10.1016/j.tice.2025.102936","DOIUrl":"10.1016/j.tice.2025.102936","url":null,"abstract":"<div><div>Acrylamide (ACR) is a hazardous contaminant posing significant hepatotoxic risks. This study investigates the hepatoprotective efficacy of quercetin-loaded nanoparticles compared to free quercetin in mitigating ACR-induced hepatotoxicity. Nanoparticles were formulated using nanoprecipitation with galactose-functionalized surfaces to enhance liver targeting. Rats were allocated into five groups: control, ACR-induced hepatotoxicity, blank nanoparticles, free quercetin, and quercetin nanoparticles. Hepatotoxicity was assessed through biochemical, molecular, histopathological, and immunohistochemical analyses, along with molecular docking studies. Results demonstrated significant elevations in hepatic enzyme levels (ALT, AST), oxidative stress markers (MDA), inflammatory mediators (MAPK, NF-κB1, NLRP3, IL-1β, IL-6), and apoptotic factors (CASP3, BAX, P53), alongside reductions in antioxidant enzymes (GSH, GPx) in the ACR group. Both quercetin treatments effectively reduced these adverse effects, with quercetin nanoparticles exhibiting superior performance, evidenced by a 25 % greater reduction in oxidative markers and a 30 % increase in antioxidant enzyme activity. Molecular docking confirmed strong interactions between quercetin and key inflammatory pathway proteins (MAPK, NF-κB, NLRP3). Enhanced bioavailability and targeted delivery contributed to the nanoparticles' superior efficacy. These findings suggest that quercetin nanoparticles significantly outperform free quercetin in ameliorating ACR-induced hepatotoxicity by attenuating oxidative stress, inflammation, and apoptosis, providing a robust foundation for their future clinical exploration.<strong>.</strong></div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102936"},"PeriodicalIF":2.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890558","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 systematic review of machine learning algorithms for breast cancer detection","authors":"Aryan Sai Boddu ,&nbsp;Aatifa Jan","doi":"10.1016/j.tice.2025.102929","DOIUrl":"10.1016/j.tice.2025.102929","url":null,"abstract":"<div><div>Breast cancer is one of the leading causes of death and morbidity among women worldwide. Identifying cancerous cells remains a complex and time-consuming task, particularly when performed manually by radiologists or pathologists, contributing to high diagnostic costs. The absence of a reliable, standardized predictive model often hinders timely and accurate diagnosis. This systematic review explores various machine learning approaches — including eXtreme Gradient Boosting (XGBoost), Naïve Bayes, Support Vector Machine (SVM), Logistic Regression, Decision Tree, and k-Nearest Neighbors (KNN) — for classifying breast tumors as malignant or benign. It synthesizes findings from existing literature, comparing model performance based on key evaluation metrics such as accuracy, precision, recall, and F1-score. Multiple reviewed studies report that machine learning models can achieve high diagnostic accuracy. These models may improve diagnostic confidence and accelerate result interpretation. This review also highlights common limitations, such as dataset availability, class imbalance, model interpretability, and generalizability across diverse populations. The paper concludes by outlining future directions to enhance the clinical applicability, trustworthiness, and integration of ML-based diagnostic systems.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102929"},"PeriodicalIF":2.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143878585","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 novel immortalization method for immortalizing human primary CD8+ T cells by inserting a single copy of human telomerase reverse transcriptase via CRISPR/Cas9","authors":"Zhiyong He,&nbsp;Kenneth D. Cole,&nbsp;Hua-Jun He","doi":"10.1016/j.tice.2025.102908","DOIUrl":"10.1016/j.tice.2025.102908","url":null,"abstract":"<div><h3>Background</h3><div>Existing cell immortalization methods made the cells obtain oncogenesis phenotype and/or caused the cells gain and/or lose chromosomes. Immortalized normal human T cells lines provide critical <em>in vitro</em> models for basic research and therapeutic products development.</div></div><div><h3>Methods</h3><div>We developed a novel method utilizing a CRISPR/Cas9 system to replace the exon 2 of the cell cycle inhibitor gene CDKN2A (encoding p16 and p14 proteins) with a single copy of human telomerase reverse transcriptase (<em>hTERT</em>) to immortalize human primary CD8⁺ T cells (hCD8⁺T-TERT).</div></div><div><h3>Results</h3><div>By using Cas9 protein and low donor DNA copies/cell, we successfully immortalized hCD8⁺T cells with a single copy of hTERT transgene, which also avoided uncontrolled insertion of Cas9 gene and guide RNA vector. Human primary CD8⁺ cells from independent donors were immortalized and expanded more than 2.6 × 10⁷ times. Characterization of one of the immortalized CD8⁺ T-TERT cell lines revealed that the cells retained most of the cell surface markers and normal karyotype. The CD8⁺ T-TERT cells also retained the dependence of IL-2 and CD3/CD28 activator for survival and expansion.</div></div><div><h3>Conclusion</h3><div>We established a stable immortalized cell lines using the novel immortalization method, and the immortalized CD8⁺ T cells had a phenotype consistent with T cells.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102908"},"PeriodicalIF":2.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890560","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":"Advances in tissue engineering utilizing microfluidic platforms and techniques","authors":"Beti Hosseinpour Ganjaroudi ,&nbsp;H.R. Ashorynejad","doi":"10.1016/j.tice.2025.102922","DOIUrl":"10.1016/j.tice.2025.102922","url":null,"abstract":"<div><div>This study aims to review the advancements in tissue engineering using microfluidic systems and techniques. In this way, tissue engineering has undergone a significant transformation through the employing of microfluidics knowledge in different areas of tissue engineering. This integration has made it possible to create biomimetic environments that more precisely resemble the physiological conditions of the human body. By using microfluidic platforms, researchers can manipulate biomaterials accurately and create complex three-dimensional (3D) scaffolds with specific characteristics. This research is devoted to illuminate the intricate, fascinating and improved collaboration between microfluidic systems and techniques such as produce high-quality hydrogels, precise vessel networks, enhanced nutrient transfer techniques, controlled hydrogel’s size have been studied. These compounds are key components in scaffold fabrication for tissue engineering. By elucidating the principles, techniques, applications and progress involved in this interface, the broadened potential of this synergistic approach in advancing the frontiers of regenerative, tissue engineering, medicine and biomedical research was uncovered.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102922"},"PeriodicalIF":2.7,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143895029","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":"The protective effect of bromelain on testicular dysfunction and oxidative stress induced by REM sleep deprivation in adult male rats","authors":"Mahboubeh Hosseinpour ,&nbsp;Amir Masoud Dalband ,&nbsp;Zahrasadat Lajevardi ,&nbsp;Arezou Soltanattar ,&nbsp;Armin Tafazolimoghadam ,&nbsp;Amin Karamian ,&nbsp;Mohammad-Amin Abdollahifar ,&nbsp;Hojjat-Allah Abbaszadeh ,&nbsp;Mahshid Hodaeipour ,&nbsp;Ali Charmchi ,&nbsp;Aliasghar Keramatinia ,&nbsp;Armin Alinezhad ,&nbsp;Fatemeh Zolfaghari ,&nbsp;Mobina Fathi ,&nbsp;Kimia Vakili ,&nbsp;Fatemeh Navaei ,&nbsp;Mojtaba Sani ,&nbsp;Pourya Raee ,&nbsp;Abbas Aliaghaei","doi":"10.1016/j.tice.2025.102927","DOIUrl":"10.1016/j.tice.2025.102927","url":null,"abstract":"<div><div>Male infertility is a significant global health concern, with sleep deprivation emerging as a potential contributing factor due to its impact on oxidative stress and reproductive function. This study investigates the protective effects of bromelain, a natural anti-inflammatory enzyme, on testicular dysfunction induced by Rapid eye movement (REM) sleep deprivation in adult male rats. Thirty-six rats were divided into control, REM sleep-deprived (REM-dep), and REM-deprived with bromelain treatment (REM-dep+Br) groups. REM sleep deprivation was induced for a 21-day period using the flower pot technique, with concurrent oral administration of bromelain (200 mg/kg) throughout this period. Finally, sperm parameters, testicular stereology, antioxidant markers (Nrf-2, γ-GCS, and GSH), and inflammatory/apoptotic markers (TNF-α, and Caspase-3) were evaluated across study groups. REM sleep deprivation significantly reduced sperm count, motility (total, and progressive), and normal morphology while increasing DNA fragmentation compared to control group. Testicular stereology revealed decreased spermatogenic cells, Sertoli cells, Leydig cells, and Johnsen scores. Bromelain administration significantly improved total sperm motility, increased spermatid numbers, and restored Leydig cell counts compared to REM-dep group. Antioxidant markers (Nrf-2, γ-GCS, GSH) were significantly reduced in the REM-dep group but restored with bromelain treatment. Immunohistochemistry showed elevated TNF-α and Caspase-3 expression in the REM-dep group, which was mitigated by bromelain administration. These findings suggest that REM sleep deprivation induces testicular dysfunction through oxidative stress and inflammation, while bromelain exerts protective effects via its antioxidant and anti-inflammatory properties. This study highlights bromelain as a potential protective /therapeutic agent for mitigating sleep deprivation-induced male reproductive dysfunction.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102927"},"PeriodicalIF":2.7,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143867746","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}