Molecular biology reports, 2024-12, Vol.51 (1), p.607-607, Article 607
2024
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- Autor(en) / Beteiligte
- Titel
- Peroxiredoxin II exerts neuroprotective effects by inhibiting endoplasmic reticulum stress and oxidative stress-induced neuronal pyroptosis
- Ist Teil von
- Molecular biology reports, 2024-12, Vol.51 (1), p.607-607, Article 607
- Ort / Verlag
- Dordrecht: Springer Netherlands
- Erscheinungsjahr
- 2024
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Background Intracerebral hemorrhage (ICH) is a critical neurological condition with few treatment options, where secondary immune responses and specific cell death forms, like pyroptosis, worsen brain damage. Pyroptosis involves gasdermin-mediated membrane pores, increasing inflammation and neural harm, with the NLRP3/Caspase-1/GSDMD pathway being central to this process. Peroxiredoxin II (Prx II), recognized for its mitochondrial protection and reactive oxygen species (ROS) scavenging abilities, appears as a promising neuronal pyroptosis modulator. However, its exact role and action mechanisms need clearer definition. This research aims to explore Prx II impact on neuronal pyroptosis and elucidate its mechanisms, especially regarding endoplasmic reticulum (ER) stress and oxidative stress-induced neuronal damage modulation. Methods and results Utilizing MTT assays, Microscopy, Hoechst/PI staining, Western blotting, and immunofluorescence, we found Prx II effectively reduces LPS/ATP-induced pyroptosis and neuroinflammation in HT22 hippocampal neuronal cells. Our results indicate Prx II’s neuroprotective actions are mediated through PI3K/AKT activation and ER stress pathway inhibition, diminishing mitochondrial dysfunction and decreasing neuronal pyroptosis through the ROS/MAPK/NF-κB pathway. These findings highlight Prx II potential therapeutic value in improving intracerebral hemorrhage outcomes by lessening secondary brain injury via critical signaling pathway modulation involved in neuronal pyroptosis. Conclusions Our study not only underlines Prx II importance in neuroprotection but also opens new therapeutic intervention avenues in intracerebral hemorrhage, stressing the complex interplay between redox regulation, ER stress, and mitochondrial dynamics in neuroinflammation and cell death management.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0301-4851eISSN: 1573-4978DOI: 10.1007/s11033-024-09568-5Titel-ID: cdi_proquest_miscellaneous_3051423448
- Format
- –
- Schlagworte
- 1-Phosphatidylinositol 3-kinase, AKT protein, Animal Anatomy, Animal Biochemistry, Animals, Biomedical and Life Sciences, Brain injury, Caspase-1, Cell death, Cell Line, Cerebral Hemorrhage - complications, Cerebral Hemorrhage - drug therapy, Cerebral Hemorrhage - metabolism, Endoplasmic reticulum, Endoplasmic Reticulum Stress - drug effects, Hemorrhage, Hippocampus, Hippocampus - metabolism, Hippocampus - pathology, Histology, Immune response, Immunofluorescence, Inflammation, Life Sciences, MAP kinase, Mice, Mitochondria, Mitochondria - drug effects, Mitochondria - metabolism, Morphology, Neuromodulation, Neurons - drug effects, Neurons - metabolism, Neuroprotection, Neuroprotective Agents - pharmacology, NF-κB protein, Original Article, Oxidative stress, Oxidative Stress - drug effects, Peroxiredoxin, Peroxiredoxins - metabolism, Pyroptosis, Pyroptosis - drug effects, Reactive oxygen species, Reactive Oxygen Species - metabolism, Signal transduction, Signal Transduction - drug effects, Stroke, Western blotting