2013
DOI: 10.1016/j.tiv.2012.12.012
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β-Ionone attenuates LPS-induced pro-inflammatory mediators such as NO, PGE2 and TNF-α in BV2 microglial cells via suppression of the NF-κB and MAPK pathway

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Cited by 42 publications
(21 citation statements)
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“…U0126, a specific inhibitor for MEK1/2, the kinases leading to phosphorylation of ERK1/2, readily abrogated IFNγ induced NO in these cells. Besides induction of ROS and NO, microglia activation is also accompanied by secretion of pro-inflammatory cytokines and chemokines, including TNFα, IL-1β and IL-6 (Kang et al, 2013; Lim, et al, 2012). Many botanical compounds offer neuroprotective effects by suppressing microglial activation.…”
Section: Discussionmentioning
confidence: 99%
“…U0126, a specific inhibitor for MEK1/2, the kinases leading to phosphorylation of ERK1/2, readily abrogated IFNγ induced NO in these cells. Besides induction of ROS and NO, microglia activation is also accompanied by secretion of pro-inflammatory cytokines and chemokines, including TNFα, IL-1β and IL-6 (Kang et al, 2013; Lim, et al, 2012). Many botanical compounds offer neuroprotective effects by suppressing microglial activation.…”
Section: Discussionmentioning
confidence: 99%
“…2 Many studies have demonstrated that activated macrophages, key inammatory cells, play a pivotal role in diseases via the secretion of various inammatory mediators such as nitric oxide (NO) and prostaglandin (PG) E2, as well as pro-inammatory cytokines, including tumor necrosis factor-a (TNF-a), interleukin-1beta (IL-1b) and interleukin-6 (IL-6). 3 Studies in animal models and patients suggest that pro-inammatory factors, including NO, TNF-a, PGE2 and IL-6 may be produced by macrophages or by the surrounding tissues, and also induce the expression of cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS), which leads to the up-regulation of NO and PGE2. 4 The activated forms of COX, namely COX-1 and COX-2, catalyze the production of leukotrienes, which are arachidonic acid metabolites.…”
Section: Introductionmentioning
confidence: 99%
“…MAPKs and NF‐κB pathways are known to play a critical role in the LPS‐induced inflammatory response in microglia . We found that Z‐590 inhibited the LPS‐stimulated MAPKs phosphorylation, including p‐ERK, p‐p38 and p‐JNK, but didn't alter the IκBα level.…”
Section: Discussionmentioning
confidence: 77%
“…Interestingly, LPS was found to alter MIF receptors expression especially CD74 and CXCR2 in BV-2 microglia (Figure 1), suggesting that MIF may also be involved MAPKs and NF-κB pathways are known to play a critical role in the LPS-induced inflammatory response in microglia. 33,34 We found that Z-590 inhibited the LPS-stimulated MAPKs phosphorylation, including p-ERK, p-p38 and p-JNK, but didn't alter the IκBα level. This was further supported by the data from nuclear expressions of p65 and p-c-Jun in BV-2 microglia cells ( Figure 4).…”
Section: Discussionmentioning
confidence: 79%