ArticleBosnian journal of basic medical sciences2016
Tocilizumab inhibits neuronal cell apoptosis and activates STAT3 in cerebral infarction rat model.
Article in Bosnian journal of basic medical sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 40 citations in OpenAlex.
- Evaluating tocilizumab in ischemic stroke: Findings from the SPAN multicenter trial.Neuropharmacology · 2026Article
- Elevated initial blood kynurenine is associated with increased odds of post-stroke infection: Kynurenine and post-stroke infection.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2025Article
- Gut Microbiota, Bacterial Translocation, and Stroke: Current Knowledge and Future Directions.Biomedicines · 2024Review
- Allopurinol is Associated with an Increased Risk of Cerebral Infarction: A Two-Sample Mendelian Randomization Study.ACS omega · 2024Article
- Tocilizumab Reduces Lung Injury in a Rat Lung Ischemia and Reperfusion Model.Thoracic research and practice · 2024Article
- The gastrointestinal-brain-microbiota axis: a promising therapeutic target for ischemic stroke.Frontiers in immunology · 2023Review
- Observation of the Effect of Nursing BPR on Thrombolytic Efficacy and Prognosis of Patients with Cerebral Infarction Based on CT Images.Contrast media & molecular imaging · 2022Article
- The Severity of Acute Kidney and Lung Injuries Induced by Cecal Ligation and Puncture Is Attenuated by Menthol: Role of Proliferating Cell Nuclear Antigen and Apoptotic Markers.Frontiers in medicine · 2022Article
- Review
- Evaluation of Preclinical and Clinical Studies Published in Medical Journals of Bosnia and Herzegovina: Methodology Issues.Acta informatica medica : AIM : journal of the Society for Medical Informatics of Bosnia & Herzegovina : casopis Drustva za medicinsku informatiku BiH · 2020Article
- Tocilizumab attenuates acute lung and kidney injuries and improves survival in a rat model of sepsis via down-regulation of NF-κB/JNK: a possible role of P-glycoprotein.Inflammopharmacology · 2020Article
- Inflammatory Profiles of the Interleukin Family and Network in Cerebral Hemorrhage.Cellular and molecular neurobiology · 2018Review
- Ulk1/FUNDC1 Prevents Nerve Cells from Hypoxia-Induced Apoptosis by Promoting Cell Autophagy.Neurochemical research · 2018Article
- Article
- Potentially Common Therapeutic Targets for Multiple Sclerosis and Ischemic Stroke.Frontiers in physiology · 2018Article
- DL-2-amino-3-phosphonopropionic acid protects primary neurons from oxygen-glucose deprivation induced injury.Bosnian journal of basic medical sciences · 2017Article
- Protective effect of TSG against oxygen-glucose deprivation in cardiomyoblast cell line H9c2: involvement of Bcl-2 family, Caspase 3/9, and Akt signaling pathway.International journal of clinical and experimental pathology · 2017Article
- Combined effects of age and polymorphisms in Notch3 in the pathogenesis of cerebral infarction disease.Metabolic brain disease · 2016Article
Corrections and comments
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral infarction is a severe hypoxic ischemic necrosis with accelerated neuronal cell apoptosis in the brain. As a monoclonal antibody against interleukin 6, tocilizumab (TCZ) is widely used in immune diseases, whose function in cerebral infarction has not been studied. This study aims to reveal the role of TCZ in regulating neuronal cell apoptosis in cerebral infarction. The cerebral infarction rat model was constructed by middle cerebral artery occlusion and treated with TCZ. Cell apoptosis in hippocampus and cortex of the brain was examined with TUNEL method. Rat neuronal cells cultured in oxygen-glucose deprivation (OGD) conditions and treated with TCZ were used to compare cell viability and apoptosis. Apoptosis-related factors including B-cell lymphoma extra large (Bcl-xL) and Caspase 3, as well as the phosphorylated signal transducer and activator of transcription 3 (p-STAT3) in brain cortex were analyzed from the protein level. Results indicated that TCZ treatment could significantly prevent the promoted cell apoptosis caused by cerebral infarction or OGD (P < 0.05 or P < 0.01). In brain cortex of the rat model, TCZ up-regulated Bcl-xL and down-regulated Caspase 3, consistent with the inhibited cell apoptosis. It also promoted tyrosine 705 phosphorylation of STAT3, which might be the potential regulatory mechanism of TCZ in neuronal cells. This study provided evidence for the protective role of TCZ against neuronal cell apoptosis in cerebral infarction. Based on these fundamental data, TCZ is a promising option for treating cerebral infarction, but further investigations on related mechanisms are still necessary.
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