Tissue & cell最新文献

{"title":"Neuroprotective effects of selenium against lithium-induced cerebellar toxicity in rats: The role of apoptosis, gliosis, and aging markers","authors":"Nora Elshehawy Helal ,&nbsp;Lashin Saad Ali ,&nbsp;Wael M. Elsaed ,&nbsp;Mohamed Berika ,&nbsp;Yasir Hassan Elhassan ,&nbsp;Khaled S. El-Bayoumi ,&nbsp;Abdelnaser A. Badawy ,&nbsp;Mosaab Salah El-din El-Agawy ,&nbsp;Amal Fahmy Dawood ,&nbsp;Mamdouh Eldesoqui","doi":"10.1016/j.tice.2025.102779","DOIUrl":"10.1016/j.tice.2025.102779","url":null,"abstract":"<div><h3>Background</h3><div>Prolonged lithium therapy in psychiatric disorders may be complicated by multi-organ dysfunction, particularly in the nervous system. Toxicity to the cerebellum is one of these, which, while uncommon, inevitably emerges negatively and permanently. Selenium is a trace element regarded as one of the critical antioxidants. Numerous investigations have validated selenium's neuroprotective properties against various neurotoxic medications. The degree of affliction of the nerve cells is assessed using GFAP, a marker of astrocytosis; Caspase-3, a marker of apoptosis; and klotho, a marker of anti-aging.</div></div><div><h3>Aim of the study</h3><div>This study is designed to investigate the cerebellar structural and functional changes in lithium-treated rats and the postulated neuroprotective role of selenium.</div></div><div><h3>Methodology</h3><div>A total of 24 adult male albino rats were divided into 4 groups: control, selenium (1 mg/kg in water solution by gavage daily), lithium (by intraperitoneal injection of 25 mg/kg lithium carbonate dissolved in 0.9 % NaCL twice daily for 4 weeks), and lithium-selenium group. Motor coordination was evaluated using the rotarod test. Cerebellar malonaldehyde (MDA) and reduced glutathione (GSH) were measured, and histopathological examination and immunohistochemical expression of Klotho, GFAP, and Caspase 3 were evaluated.</div></div><div><h3>Results</h3><div>The lithium-treated group exhibited reduced latency on the rotarod test, elevated oxidative stress indicators, and an altered cerebellar structure in HE and cresyl violet-stained sections. Moreover, there was a diminished Klotho expression and increased levels of both caspase-3 and GFAP expression. Selenium administration reduced latency time, diminished oxidative stress markers, mitigated lithium-induced cerebellar alterations, increased Klotho expression, and lowered the expression of caspase-3 and GFAP.</div></div><div><h3>Conclusion</h3><div>Lithium exposure causes alterations in the cerebellar cortical structure in albino rats. Selenium protected the cerebellar cortex from such changes by enhancing Klotho expression, diminishing oxidative stress, and reducing apoptosis.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102779"},"PeriodicalIF":2.7,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419241","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":"Autonomic nervous system imbalance in diabetic mouse choroids","authors":"Yuan-jun Qin ,&nbsp;Yong-Chao Zhang ,&nbsp;Yunru Lin ,&nbsp;Yiyi Hong ,&nbsp;Xufang Sun ,&nbsp;Fan Xu ,&nbsp;Changzheng Chen","doi":"10.1016/j.tice.2025.102798","DOIUrl":"10.1016/j.tice.2025.102798","url":null,"abstract":"<div><h3>Purpose</h3><div>We investigated neurohomeostasis and its possible underlying mechanisms in the choroids of diabetic mice.</div></div><div><h3>Methods</h3><div>Streptozotocin-induced diabetic mice were used in this study. Choroidal nerve fiber alterations were observed via transmission electron microscopy (TEM). The levels of epinephrine and acetylcholine in the choroid were determined via ultra-high-performance liquid chromatography–tandem mass spectrometry. Tyrosine hydroxylase (TH), choline acetyl transferase (ChAT), and neuronal nitric oxide synthase (nNOS), vasoactive intestinal peptide (VIP), neuropeptide Y (NPY), and calcitonin gene-related peptide (CGRP) levels were evaluated by western blot or quantitative real-time polymerase chain reaction. In addition, immunofluorescence staining were used to analyze the changes in key enzymes (TH, dopamine beta-hydroxylase (DβH), and CGRP) in the superior cervical sympathetic ganglia (SCG) and trigeminal ganglia (TG).</div></div><div><h3>Results</h3><div>TEM revealed a loose myelin sheath around nerve fibers, axon atrophy, and cytoplasmic vacuoles in Schwann cells in diabetic choroids. Lower epinephrine levels were observed in diabetic mice. Although no difference was found in acetylcholine level, the epinephrine-to-acetylcholine ratio was greatly decreased. Decreased TH and increased ChAT, nNOS, VIP, NPY, and CGRP were found in diabetic choroids. Fewer TH-positive and DβH-positive neuronal cells were found in the SCGs of diabetic mice. More CGRP-positive and fewer TH-positive neuronal cells were observed in the TG of diabetic mice.</div></div><div><h3>Conclusions</h3><div>Altered markers of the sympathetic, parasympathetic and sensory systems were present in diabetic mouse choroids. An imbalanced choroidal nervous system might explain the initiation of choroidal neovascularization in diabetic patients.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102798"},"PeriodicalIF":2.7,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143436429","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":"GIT2 negatively regulates the NF-κB pathway directly or indirectly by regulating TRAF3 expression to promote osteogenic differentiation of BMSCs","authors":"Yanna Wang ,&nbsp;Changyuan Wang ,&nbsp;Ying Gong ,&nbsp;Qingchen Li ,&nbsp;Mozhen Liu ,&nbsp;Huijun Sun","doi":"10.1016/j.tice.2025.102790","DOIUrl":"10.1016/j.tice.2025.102790","url":null,"abstract":"<div><h3>Background aims</h3><div>Osteoporosis (OP) is a common disease of aging, which is closely related to the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). DNA damage, as a senescence-associated secretory phenotype (SASP), plays an important role in aging diseases including OP. GIT2 has been identified as a DNA repair gene and alleviates aging-related phenotypes. However, the relationship between GIT2 and osteogenic differentiation of BMSCs remains unclear.</div></div><div><h3>Methods</h3><div>Here, we used bioinformatics analysis to identify the gene GIT2, which is closely related to aging, OP and DNA damage, and its downstream targets. Then, H₂O₂ -induced BMSCs senescence model and ovariectomy-induced mice OP model was established in vitro and in vivo, respectively. Micro-CT, H&amp;E staining, toluidine blue staining, and calcein double labeling were used to analyze bone mass, osteogenic differentiation phenotype, and bone formation rate. Comet assay, Elisa and immunofluorescence were used to analyze senescence-related phenotypes. Western blotting was used to detect the protein levels of GIT2/TRAF3/NF-κB axis and osteogenesis-related markers.</div></div><div><h3>Results</h3><div>Our results showed that GTI2 and TRAF3 were positively correlated with OP-related markers. On the one hand, GIT2 could inhibit the activation of both canonical and non-canonical NF-κB signaling pathways by positively regulating TRAF3. On the other hand, GIT2 could directly bind to P65, a component of the classical NF-κB signaling pathway, and P52, a component of the non-classical NF-κB signaling pathway, to inhibit their activation, improve DNA damage repair, alleviate cell senescence, and further promote osteogenic differentiation of BMSCs.</div></div><div><h3>Conclusions</h3><div>In summary, the present study demonstrates that GIT2 plays a crucial regulatory role in promoting osteogenic differentiation of BMSCs, which provides new ideas for the prevention and treatment of OP and other aging-related diseases.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102790"},"PeriodicalIF":2.7,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419128","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":"Ferrostatin-1 mitigates acute lung injury by reducing ferroptosis levels in gas explosions","authors":"Hao Zhang ,&nbsp;Linqiang Tian ,&nbsp;Peng Wang ,&nbsp;Long Li ,&nbsp;Kunxi Wang ,&nbsp;Yanyan Li ,&nbsp;Yue Zhang ,&nbsp;Lili Feng ,&nbsp;Sanqiao Yao ,&nbsp;Hao Guan ,&nbsp;Wenjie Ren","doi":"10.1016/j.tice.2025.102773","DOIUrl":"10.1016/j.tice.2025.102773","url":null,"abstract":"<div><h3>Background</h3><div>Gas explosion injuries are a severe form of trauma with high incidence and mortality rates, both in daily life and industrial settings. Acute lung injury (ALI) is one of the most serious complications of gas explosion injuries and is a leading cause of mortality in such cases. However, the mechanisms underlying gas explosion-induced ALI have not been fully elucidated, and the treatment process consumes a significant amount of medical resources. Therefore, it is crucial to conduct research on the injury mechanisms of gas explosion injuries, especially the mechanisms of gas explosion-induced ALI, which can effectively improve the treatment rate of this condition. In this study, we analyzed the relationship between a novel form of cell death, ferroptosis, and gas explosion-induced ALI, and explored its specific mechanisms.</div></div><div><h3>Methods</h3><div>We established ALI rat model by Shock tube biological injury system, and detected lung injury-related indexes as well as ferroptosis related indexes, such as glutathione peroxidase 4（GPX4）, 4-hydroxynonenal（4HNE）, Malondialdehyde（MDA）, Fe2 + . We also investigated the therapeutic effects of the ferroptosis inhibitor ferrostatin-1 (Fer-1) in ALI induced by gas explosion, as well as its specific mechanisms of action.</div></div><div><h3>Results</h3><div>A rat ALI model by gas explosion was successfully established. After the gas explosion treatment, we observed that the systemic inflammatory reaction of rats was increased, and lung function, liver function, kidney function and cardiac function were damaged to different degrees. The inflammatory infiltration in the lung tissue was more severe, and the degree of lung injury and pulmonary edema increased. The ferroptosis markers GPX4 was decreased, while the levels of 4HNE, MDA and Fe2 + were increased. Treatment with Fer-1 significantly ameliorated gas explosion ALI damage and down-regulated the expression level of ferroptosis.</div></div><div><h3>Conclusions</h3><div>Gas explosion-induced ALI in rats is characterized by enhanced inflammatory responses and reduced antioxidant capacity in lung tissues. The specific mechanism of injury involves ferroptosis. Fer-1 has been shown to mitigate the severity of ALI caused by gas explosion by suppressing ferroptosis expression levels in lung tissues via the Nrf2/GPX4 axis.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102773"},"PeriodicalIF":2.7,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419242","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 significance of the activating transcription factor 6 gene in the pathogenesis of drug resistant cancer","authors":"Ashkan Khanishayan ,&nbsp;Soheila Rahgozar ,&nbsp;Diba Zebardast","doi":"10.1016/j.tice.2025.102786","DOIUrl":"10.1016/j.tice.2025.102786","url":null,"abstract":"<div><div>Chemotherapy remains a cornerstone in cancer therapy, but its effectiveness is often hindered by the development of drug resistance, a significant factor contributing to over 90 % of cancer-related deaths worldwide. A critical aspect of this resistance involves chronic endoplasmic reticulum stress, which activates the unfolded protein response (UPR), mainly through the activation of Activating Transcription Factor 6 (ATF6). Elevated ATF6 expression has been found to correlate with poor survival outcomes and increased resistance to chemotherapy across several malignancies. This study specifically investigates the role of ATF6 in cancer pathogenesis, focusing on its involvement in resistance mechanisms and the progression of the disease. Given the complex interactions between the UPR and other cellular pathways, including the DNA damage response (DDR), our findings emphasize the potential of targeting ATF6 and UPR and DDR pathways as a novel therapeutic strategy. This approach could potentially overcome chemoresistance and improve outcomes in cancer treatment.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102786"},"PeriodicalIF":2.7,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143386563","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":"Targeting DUSP3 promotes cell senescence by activating the notch1 pathway to treat hepatocellular carcinoma","authors":"Wen-Jun Zhang,&nbsp;Jun-Lu Peng,&nbsp;Da-Fei Dai,&nbsp;Chen Huang,&nbsp;Xiao-Peng Chen","doi":"10.1016/j.tice.2025.102781","DOIUrl":"10.1016/j.tice.2025.102781","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) is a malignant tumor of the digestive system, influenced by various factors. Due to its subtle clinical symptoms, it delayed results in poor prognosis and limited treatment options. Cellular senescence, characterized by stable growth arrest, is closely linked to tumor proliferation inhibition, making it a promising therapeutic strategy for HCC. However, the role of Dual Specificity Phosphatase 3 (DUSP3) in HCC-induced senescence and its underlying mechanisms remain poorly understood. Our preliminary data show a marked upregulation of DUSP3 in HCC tissues compared to adjacent group. Additionally, DUSP3 knockdown induced senescence in HCC cells in vitro. Further investigation revealed that inhibiting Notch1 reversed the senescence induced by DUSP3 knockdown in these cells. Thus, targeting DUSP3 to activate the Notch1 pathway and induction of senescence as a promising anti-tumor strategy.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102781"},"PeriodicalIF":2.7,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Status epilepticus alters hippocampal ultrastructure in kainic acid rat model","authors":"Mzia G. Zhvania ,&nbsp;Irina Sharikadze ,&nbsp;Nadezhda Japaridze ,&nbsp;Yousef Tizabi ,&nbsp;Fuad Rzayev ,&nbsp;Eldar Gasimov ,&nbsp;Giorgi Lobzhanidze","doi":"10.1016/j.tice.2025.102789","DOIUrl":"10.1016/j.tice.2025.102789","url":null,"abstract":"<div><div>Kainic acid (KA) model of epilepsy is a reliable tool to study temporal lobe epilepsy (TLE), the most common type of partial epilepsy in adults. Substantial body of data suggest that the KA-induced status epilepticus (SE) leads to several molecular and structural changes in the hippocampus, including sclerosis, sprouting of mossy fiber, reorganization of inter-neuronal networks, alterations in neuropeptide signaling, gliosis, and synaptic transmission dysregulation. However, no details on the ultrastructural changes, especially in relationship to synapses are available. This information is important in providing a comprehensive understanding of subtle changes that occur in this debilitating disease. Thus, in this study, applying electron-microscopic morphometric analysis, we evaluated the ultrastructural effects of KA on the CA1 region of the hippocampus, an area intimately involved in SE. The total number of synaptic vesicles (SVs), the number of docking SVs, the length of synapse active zone (AZ) and the number and area of presynaptic and postsynaptic mitochondria in axo-dendritic (excitatory) synapses were measured at 24 h, and 8 and 21 days after KA administration. Results indicate a decrease in the total number and docking of SVs, an increase in the length of AZ and the number and area of presynaptic and postsynaptic mitochondria, which were more prominent at 8 days after KA injection. The findings suggest a time-dependent ultrastructural changes in CA1 region of the hippocampus in an animal model of focal epilepsy.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102789"},"PeriodicalIF":2.7,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419131","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":"Immunolocalization of cell proliferation and tumor markers in the regenerating tail of the lizard Podarcis muralis likely involved in cell proliferation control.","authors":"Lorenzo Alibardi","doi":"10.1016/j.tice.2025.102782","DOIUrl":"https://doi.org/10.1016/j.tice.2025.102782","url":null,"abstract":"<p><strong>Purpose: </strong>The lizard blastema expresses typical genes present in cancer cells, and CD44 and S100A4 markers are known to be associated with metastasis, a process that is absent during tail regeneration in lizard.</p><p><strong>Method: </strong>The present immunohistochemical study analyzes the distribution of hyaluronate, its main receptor CD44, and S100A4 (metastasin-1) in relation to proliferating cells in the early regenerating tail of the lizard Podarcis muralis.</p><p><strong>Results: </strong>The regenerating blastema contains sparse proliferating cells immersed in a hyaluronate-rich extracellular matrix and these cells show a diffuse labeling for CD44 and S100A4. These proteins are more intensely localized in the apical regenerating (wound) epidermis and ependymal ampulla (regenerating spinal cord), two tissues essential for the stimulation of tail regeneration in lizards. Both markers generally show a cytoplasmic localization, but also a nuclear labeling is present in basal cells of the regenerating epidermis in the blastema, especially for S100A4. The latter protein is highly expressed in differentiating epidermis of regenerating scales, especially in the forming beta-layer.</p><p><strong>Conclusions: </strong>The expression of these two marker oncoproteins, however, like others previously studied, is not associated with metastasis in the lizard blastema that instead develops into a new tail. The activation of cancer marker genes and proteins in the regenerating blastema does not determine degeneration into a tumor outgrowth. This process remains so far unexplained but is worth of a detailed molecular and cellular analysis aiming to find key processes on this physiological mechanism of tumor self-remission.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"102782"},"PeriodicalIF":2.7,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143410880","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":"Application of mRNA technology in neuronal protection of human mature brain-derived neurotrophic factor.","authors":"Liang Wang, Fengjuan Su, Heng Huang, Qiuhong Jiang, Haifang Kong, Zhong Pei","doi":"10.1016/j.tice.2025.102788","DOIUrl":"https://doi.org/10.1016/j.tice.2025.102788","url":null,"abstract":"<p><strong>Background: </strong>Although human mature brain-derived neurotrophic factor (hmBDNF) offers potential neuronal protection, its clinical translation remains challenging. Messenger RNA (mRNA) technology is promising in selectively upregulating protein cleavage products. This proof-of-concept study aims to evaluate the neuronal protective effects of hmBDNF mRNA in vitro.</p><p><strong>Methods: </strong>We optimized and synthesized hmBDNF mRNA and conducted dose-response and time-response analyses in SH-SY5Y cells. mRNA expression was assessed via qPCR, while protein expression was evaluated through immunostaining and ELISA. Cell survival rate was measured using cell counting kit-8. We examined cell survival rates in both differentiated and non-differentiated SH-SY5Y cells exposed to H2O2 or serum deprivation following hmBDNF mRNA incubation. Additionally, we assessed the expression of synapse-relevant genes (MAP2, synaptophysin) and the mBDNF receptor (TrkB) in both cell types.</p><p><strong>Results: </strong>The optimized hmBDNF mRNA effectively upregulated hmBDNF expression in SH-SY5Y cells with minimal impact on endogenous proBDNF expression. Dose-response and time-response analyses identified the optimal dose and time point for maximum hmBDNF expression. hmBDNF mRNA significantly increased cell survival in differentiated SH-SY5Y cells expressing MAP2, synaptophysin and TrkB after exposure to oxidative stress or serum deprivation. However, hmBDNF mRNA did not enhance cell survival in non-differentiated SH-SY5Y cells.</p><p><strong>Conclusion: </strong>The optimized hmBDNF mRNA demonstrated a capacity for neuronal protection in vitro. Further in-vivo studies are required to assess its potential for clinical translation.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"102788"},"PeriodicalIF":2.7,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143400074","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":"Possible therapeutic effects of PROK2 in testicular ischemia/reperfusion injury: A preclinical study in Wistar albino rats.","authors":"Ilayda Uysal, Nesibe Yilmaz, Semir Gul, Kevser Tanbek, Umit Yilmaz","doi":"10.1016/j.tice.2025.102778","DOIUrl":"https://doi.org/10.1016/j.tice.2025.102778","url":null,"abstract":"<p><p>This study aimed to investigate the therapeutic effects of PROK2 on oxidative stress, inflammatory response, and tissue damage caused by ischaemia/reperfusion (I/R) in testicular tissue. A total of 48 prepubertal male Wistar albino rats were divided into four groups: sham, testicular torsion/detorsion (TTD), testicular torsion + PROK2 + detorsion (TT + PROK2 + TD), and testicular torsion/detorsion + PROK2 (TTD + PROK2) (n = 12). Testicular torsion/detorsion surgeries (2 hours of torsion followed by 24 hours of detorsion) were performed on all groups except the sham group. The TT + PROK2 + TD group received a single dose of PROK2 (60 nmol/kg) intraperitoneally 30 minutes before the end of torsion, while the TTD + PROK2 group received a single dose of PROK2 (60 nmol/kg) at the beginning of detorsion. Subsequently, biochemical parameters (serum testosterone level, total antioxidant capacity (TAS), total oxidant capacity (TOS), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) levels in testicular tissue), as well as histopathological and immunohistochemical changes, were evaluated. In TTD, a significant decrease was observed in testosterone and TAS levels, while there was an increase in TOS, TNF-α, and IL-6 levels. PROK2 treatment reduced inflammatory parameters and enhanced antioxidant parameters and testosterone levels. Additionally, a low Johnsen's score and spermatogonia count in the TTD group improved with PROK2 treatment. We concluded that PROK2, by exhibiting antioxidative and anti-inflammatory properties, may have a therapeutic effect on I/R-induced tissue damage in testicular tissue.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"102778"},"PeriodicalIF":2.7,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143415296","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}