Osmotin attenuates LPS-induced neuroinflammation and memory impairments via the TLR4/NF kappa B signaling pathwayopen access
- Authors
- Badshah, Haroon; Ali, Tahir; Kim, Myeong Ok
- Issue Date
- 20-Apr-2016
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- SCIENTIFIC REPORTS, v.6
- Indexed
- SCIE
SCOPUS
- Journal Title
- SCIENTIFIC REPORTS
- Volume
- 6
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/15534
- DOI
- 10.1038/srep24493
- ISSN
- 2045-2322
- Abstract
- Toll-like receptor 4 (TLR4) signaling in the brain mediates autoimmune responses and induces neuroinflammation that results in neurodegenerative diseases, such as Alzheimer's disease (AD). The plant hormone osmotin inhibited lipopolysaccharide (LPS)-induced TLR4 downstream signaling, including activation of TLR4, CD14, IKK alpha/beta, and NF kappa B, and the release of inflammatory mediators, such as COX-2, TNF-alpha, iNOS, and IL-1 beta. Immunoprecipitation demonstrated colocalization of TLR4 and AdipoR1 receptors in BV2 microglial cells, which suggests that osmotin binds to AdipoR1 and inhibits downstream TLR4 signaling. Furthermore, osmotin treatment reversed LPS-induced behavioral and memory disturbances and attenuated LPS-induced increases in the expression of AD markers, such as A beta, APP, BACE-1, and p-Tau. Osmotin improved synaptic functionality via enhancing the activity of pre-and post-synaptic markers, like PSD-95, SNAP-25, and syntaxin-1. Osmotin also prevented LPS-induced apoptotic neurodegeneration via inhibition of PARP-1 and caspase-3. Overall, our studies demonstrated that osmotin prevented neuroinflammation-associated memory impairment and neurodegeneration and suggest AdipoR1 as a therapeutic target for the treatment of neuroinflammation and neurological disorders, such as AD.
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