{"title":"Neuroprotective effects of tranexamic acid against hydrogen peroxide-induced cytotoxicity on human neuroblastoma SH-SY5Y cells.","authors":"Ali Niapour, Yavar Mohebi, Hossein Ghalehnoei","doi":"10.1080/01616412.2025.2462030","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Tranexamic acid (TA) is an anticoagulant drug that is used worldwide. However, the adverse effects of TA may insult the nervous system. This study aimed to investigate the dual effects of TA on SH-SY5Y cells, including its detrimental and neuroprotective effects.</p><p><strong>Methods: </strong>SH-SY5Y cells were treated with various concentrations of TA and exposed to H2O2 for 24 hours. The neuroprotective effects of TA were evaluated in H2O2-challenged cells. To assess the neuroprotective effects of TA, SH-SY5Y cells were pretreated with TA for 12 hours and then exposed to H2O2 for 24 hours. Cell viability was assessed using the MTT assay. Flow cytometry was used to evaluate cellular apoptosis. The expression of Bax, Bcl-2, and Caspase-3 genes was analyzed by real-time PCR. Additionally, Akt phosphorylation was evaluated using western blotting.</p><p><strong>Results: </strong>At high concentrations, TA reduced cell viability and induced apoptosis by up-regulating BAX and Caspase-3 gene expression and down-regulating BCL-2 transcript. Furthermore, Akt phosphorylation was reduced following TA treatment. TA exhibited protective effects against H2O2-induced cell stress by down-regulating Bax and Caspase-3 gene expression, up-regulating Bcl-2 expression, and increasing the p-AKT/AKT ratio.</p><p><strong>Conclusion: </strong>Our findings demonstrated that TA exerts its neuroprotective effect at lower concentrations, but induces apoptosis in SH-SY5Y cells at high concentrations.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-9"},"PeriodicalIF":1.7000,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurological Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/01616412.2025.2462030","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction: Tranexamic acid (TA) is an anticoagulant drug that is used worldwide. However, the adverse effects of TA may insult the nervous system. This study aimed to investigate the dual effects of TA on SH-SY5Y cells, including its detrimental and neuroprotective effects.
Methods: SH-SY5Y cells were treated with various concentrations of TA and exposed to H2O2 for 24 hours. The neuroprotective effects of TA were evaluated in H2O2-challenged cells. To assess the neuroprotective effects of TA, SH-SY5Y cells were pretreated with TA for 12 hours and then exposed to H2O2 for 24 hours. Cell viability was assessed using the MTT assay. Flow cytometry was used to evaluate cellular apoptosis. The expression of Bax, Bcl-2, and Caspase-3 genes was analyzed by real-time PCR. Additionally, Akt phosphorylation was evaluated using western blotting.
Results: At high concentrations, TA reduced cell viability and induced apoptosis by up-regulating BAX and Caspase-3 gene expression and down-regulating BCL-2 transcript. Furthermore, Akt phosphorylation was reduced following TA treatment. TA exhibited protective effects against H2O2-induced cell stress by down-regulating Bax and Caspase-3 gene expression, up-regulating Bcl-2 expression, and increasing the p-AKT/AKT ratio.
Conclusion: Our findings demonstrated that TA exerts its neuroprotective effect at lower concentrations, but induces apoptosis in SH-SY5Y cells at high concentrations.
期刊介绍:
Neurological Research is an international, peer-reviewed journal for reporting both basic and clinical research in the fields of neurosurgery, neurology, neuroengineering and neurosciences. It provides a medium for those who recognize the wider implications of their work and who wish to be informed of the relevant experience of others in related and more distant fields.
The scope of the journal includes:
•Stem cell applications
•Molecular neuroscience
•Neuropharmacology
•Neuroradiology
•Neurochemistry
•Biomathematical models
•Endovascular neurosurgery
•Innovation in neurosurgery.