Abstract
Microglia are the resident immune cells in the central nervous system (CNS), which play important roles in the repair of neuroinflammatory injury. The present study investigated the anti-neuroinflammatory effects of vinpocetine induced by lipopolysaccharide (LPS) in BV2 microglia. BV2 microglia were pretreated with vinpocetine, and then stimulated with LPS (100 ng/mL). The cytotoxicity of BV2 microglia was assessed by MTT assay. The expression levels of nitrite oxide were measured by Griess assay. Proinflammatory cytokines and mediators were determined by Western blot, ELISA, or quantitative real-time PCR. Vinpocetine significantly decreased the generation of nitric oxide-inducible nitric oxide synthase (iNOS), cyclooxygenase- (COX-) 2 in a dose-dependent manner. In addition, vinpocetine decreased the production of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin (IL)-6 and IL-1β. Furthermore, it was observed that phosphorylation levels of AMPK (Thr-172) decreased in LPS-stimulated BV2 microglia. Vinpocetine treatment increased AMPK phosphorylation in LPS-stimulated BV2 microglia. AMPK inhibition by siRNA blocked the anti-inflammatory effects of vinpocetine induced by LPS in BV2 microglia. The overall results demonstrate that vinpocetine has anti-inflammatory effects on LPS-stimulated BV2 microglia via inducing phosphorylation of AMPK, suggesting that vinpocetine is a potential therapeutic agent in neuroinflammatory injury.
Highlights
Microglia cells constitute 10-15% of the glial cell population in mammal adult brain, which originate as primitive macrophages from the embryonic yolk sac (Subhramanyam et al 2019)
Vinpocetine reduces the generation of NO in LPS-stimulated BV2 microglia
We found that vinpocetine did not influence the viability of BV2 microglia up to 50 μM (Figure 1a)
Summary
Microglia cells constitute 10-15% of the glial cell population in mammal adult brain, which originate as primitive macrophages from the embryonic yolk sac (Subhramanyam et al 2019). Microglia cells are the first line of defense against pathogens or injury in the brain. In response to brain injury, microglia cells can produce inflammatory factors such as iNOS, COX-2, Interleukin-1β (IL-1β), Interleukin-6. Adenosine monophosphate-activated protein kinase (AMPK) is a highly conserved serine/threonine protein kinase, which is regulated by the AMP/ATP ratio to restore the energy balance (Garcia & Shaw 2017). AMPK is a key regulator of immunity and inflammation, which suppresses the expression of inflammatory genes through multiple downstream pathways such as nuclear factor kB (NF-kB) and toll-like receptors (Vaez et al 2016). The regulatory effect of AMPK on neuroinflammatory response has attracted much attention (Zheng et al 2019, Harun-Or-Rashid & Inman 2018)
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