Edaravone attenuates hippocampal damage in an infant mouse model of pneumococcal meningitis by reducing HMGB1 and iNOS expression via the Nrf2/HO-1 pathway.

作者: Zheng Li , Qian-qian Ma , Yan Yan , Feng-dan Xu , Xiao-ying Zhang

DOI: 10.1038/APS.2016.71

关键词:

摘要: Aim: Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one) is a free radical scavenger that has shown potent antioxidant, anti-inflammatory and neuroprotective effects in variety of disease models. In this study, we investigated whether edaravone produced actions an infant mouse model pneumococcal meningitis. Methods: C57BL/6 mice were infected on postnatal d 11 by intracisternal injection certain inoculum Streptococcus pneumoniae . The received 10 μL saline containing (3 mg/kg) once day for 7 d. severity meningitis was assessed with clinical score. severe meningitis, the survival rate from time infection to 8 after analyzed using Kaplan-Meier curves. mild CSF inflammation cytokine levels hippocampus infection, neurological deficit score evaluated scoring system 14 infection. nuclear factor (erythroid-derived 2)-like 2 knockout (Nrf2 KO) heme oxygenase-1 (HO-1 used confirm involvement Nrf2/HO-1 pathway edaravone. Results: treatment significantly increased (76.4%) compared group (32.2%). decreased number leukocytes TNF- CSF, as well neuronal apoptosis protein HMGB1 iNOS hippocampus, but did not affect high IL-10 IL-6 hippocampus. Moreover, improved function meningitis. Nrf2 KO or HO-1 no longer effective improving (20.2% 53.6%, respectively), nor it affected Conclusion: produces reducing expression via pathway. Thus, may be promising agent bacterial

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