• Neuroscience · May 2022

    Vanillin attenuates proinflammatory factors in a tMCAO mouse model via inhibition of TLR4/NF-kB signaling pathway.

    • Ping Wang, Chunyi Li, Guolei Liao, Yihuan Huang, Xuxian Lv, Xudong Liu, Wenli Chen, and Lei Zhang.
    • Sun Yat-Sen University, The Fifth Affiliated Hospital, Department of Cerebrovascular Disease, Zhuhai 519000, Guangdong, People's Republic of China.
    • Neuroscience. 2022 May 21; 491: 65-74.

    AbstractVanillin has been reported to reduce hippocampal neuronal death in rat models of global cerebral ischemia. However, the immunoregulatory mechanism of vanillin in ischemic stroke is still unclear. To investigate the role of vanillin in a mouse model of ischemic stroke, we administered vanillin to mice after transient middle cerebral artery occlusion (tMCAO) by tail vein injection. Vanillin reduced infarct volume and improved motor function in mice after ischemia and reperfusion. IL-1β and TNF-α were decreased in ischemic brain tissue of tMCAO mice after vanillin treatment compared with saline treatment. Similar effects were observed using the in vitro LPS-stimulated microglia cell model. Moreover, the reduced expression of proinflammatory cytokines in the vanillin group was related to TLR4/NF-κB signaling. Taken together, the findings suggest that vanillin decreased microglial activation by inhibiting the TLR4 /NF-κB signaling pathway, which reduced expression of proinflammatory cytokines IL-1β and TNF-α, and finally reduced the infarct volume and improved motor function in tMCAO mice.Copyright © 2022 IBRO. Published by Elsevier Ltd. All rights reserved.

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