Corrigendum: Dl-3-n-Butylphthalide Exerts Dopaminergic Neuroprotection Through Inhibition of Neuroinflammation
Autor: | Yun-Cheng Wu, Xuan Li, Sheng-Han Kuo, Mei Yu, Xiaoying Zhu, Ting-Ting Wu, Fang Huang, Qing Li, Heng Li, Yajing Chen |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Aging Cognitive Neuroscience Parkinson's disease microglia Pharmacology Neuroprotection NF-κB lcsh:RC321-571 neuroinflammation 03 medical and health sciences 0302 clinical medicine dl-3-n-butylphthalide medicine Viability assay lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry PI3K/AKT/mTOR pathway Neuroinflammation Original Research Microglia Chemistry Neurodegeneration Dopaminergic Neurotoxicity Correction medicine.disease MAPK 030104 developmental biology medicine.anatomical_structure Parkinson’s disease 030217 neurology & neurosurgery Neuroscience |
Zdroj: | Frontiers in Aging Neuroscience Frontiers in Aging Neuroscience, Vol 11 (2019) |
ISSN: | 1663-4365 |
Popis: | Microglia-mediated neuroinflammation contributes to multiple neurodegenerative disorders, including PD. Therefore, the regulation of microglial activation probably has the therapeutic potential. This study is aimed to determine whether NBP could suppress microglial activation and protect dopaminergic neurons from excessive neuroinflammation. In the present study, MPTP-induced PD model was established to explore the neuroprotective and anti-inflammatory effect of NBP. We assessed motor deficits, dopaminergic neurodegeneration and microglial activation in PD mice. In vitro, the anti-inflammatory activity of NBP was confirmed by cell viability assay of SH-SY5Y cells after being treated with conditioned medium from LPS-stimulated BV-2 cells and from 1-Methyl-4-phenylpyridinium iodide (MPP+)-stimulated BV-2 cells. The expression of pro-inflammatory molecules was determined by RT-PCR, Western Blot and ELISA assay. The generation of NO and ROS were also assessed. The involvement of signaling pathways such as MAPK, NF-κB, and PI3k/Akt were further investigated by Western Blot and immunofluorescence assay. The neuroprotective effect of NBP was demonstrated in vivo as shown by the improvement of dopaminergic neurodegeneration, motor deficits and microglial activation in MPTP-induced mouse model of PD. The expression of pro-inflammatory mediators was also reduced by NBP administration. In vitro, NBP also protected dopaminergic neurons from neurotoxicity induced by activated microglia. NBP pretreatment not only reduced pro-inflammatory molecules, but also suppressed NO release and ROS generation in BV-2 cells. Further mechanism research suggested that the inactivation of MAPK, NF-κB and PI3K/Akt may involve in anti-neuroinflammation role of NBP. In conclusion, our results revealed that NBP exerted dopaminergic neuroprotection through inhibition of microglia-mediated neuroinflammation, suggesting the promising therapeutic effect of NBP for PD. |
Databáze: | OpenAIRE |
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