Abstract
BackgroundInflammation has been found to be associated with many neurodegenerative diseases, including Parkinson’s and dementia. Attenuation of microglia-induced inflammation is a strategy that impedes the progression of neurodegenerative diseases.MethodsWe used lipopolysaccharide (LPS) to simulate murine microglia cells (BV2 cells) as an experimental model to mimic the inflammatory environment in the brain. In addition, we examined the anti-inflammatory ability of corylin, a main compound isolated from Psoralea corylifolia L. that is commonly used in Chinese herbal medicine. The production of nitric oxide (NO) by LPS-activated BV2 cells was measured using Griess reaction. The secretion of proinflammatory cytokines including tumor necrosis factor (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) by LPS-activated BV2 cells was analyzed using enzyme-linked immunosorbent assay (ELISA). The expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3), apoptosis-associated speck-like protein containing a caspase-activation and recruitment domain (ASC), caspase-1, IL-1β and mitogen-activated protein kinases (MAPKs) in LPS-activated BV2 cells was examined by Western blot.ResultsOur experimental results demonstrated that corylin suppressed the production of NO and proinflammatory cytokines by LPS-activated BV2 cells. In addition, corylin inhibited the expression of iNOS and COX-2, attenuated the phosphorylation of ERK, JNK and p38, decreased the expression of NLRP3 and ASC, and repressed the activation of caspase-1 and IL-1β by LPS-activated BV2 cells.ConclusionOur results indicate the anti-inflammatory effects of corylin acted through attenuating LPS-induced inflammation and inhibiting the activation of NLRP3 inflammasome in LPS-activated BV2 cells. These results suggest that corylin might have potential in treating brain inflammation and attenuating the progression of neurodegeneration diseases.
Highlights
Inflammation has been found to be associated with many neurodegenerative diseases, including Parkinson’s and dementia
Corylin inhibits the production of nitric oxide (NO) and the expression of inducible NO synthase (iNOS) and COX-2 in LPS-activated murine microglial cells To avoid the toxic effects of corylin, we performed MTT assay to examine the cell survival after corylin and LPS
We further examined the effect of corylin on the expression of iNOS and COX-2 using Western blot
Summary
Inflammation has been found to be associated with many neurodegenerative diseases, including Parkinson’s and dementia. Inflammation has been found to be associated with pathogenesis of various neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease [1]. The activated microglia secrete several inflammatory cytokines and neurotoxic mediators such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and nitric oxide (NO), while augmenting neurodegeneration and neuronal death [5,6,7]. TLR4 recognizes extracellular deposits of insoluble amyloid-β, which is a pivotal contributor to Alzheimer’s disease, and activates microglia [8]. TLR4 activation critically contributes to neurodegeneration and neuronal death [9, 10], and is involved in development of neurodegenerative diseases [11, 12]
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