2016
DOI: 10.1016/j.neulet.2016.05.066
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The reciprocal interaction of sympathetic nervous system and cAMP-PKA-NF-kB pathway in immune suppression after experimental stroke

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Cited by 43 publications
(35 citation statements)
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“…Compared with 24 and 48 h after pMCAO, the motor function of rats shows slight recovery at 72 h in rotarod test [32]. The levels of transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) and of heme oxygenase-1 (HO-1) peak at 24 h and decrease at 72 h after ischemia, and NF-jB is also down-regulated at 72 h [33,34]. In addition, the serum level of the proinflammatory factor TNF-a is decreased, while that of the anti-inflammatory cytokine IL-10 is increased at 72 h after ischemia [34].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Compared with 24 and 48 h after pMCAO, the motor function of rats shows slight recovery at 72 h in rotarod test [32]. The levels of transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) and of heme oxygenase-1 (HO-1) peak at 24 h and decrease at 72 h after ischemia, and NF-jB is also down-regulated at 72 h [33,34]. In addition, the serum level of the proinflammatory factor TNF-a is decreased, while that of the anti-inflammatory cytokine IL-10 is increased at 72 h after ischemia [34].…”
Section: Discussionmentioning
confidence: 99%
“…The levels of transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) and of heme oxygenase-1 (HO-1) peak at 24 h and decrease at 72 h after ischemia, and NF-jB is also down-regulated at 72 h [33,34]. In addition, the serum level of the proinflammatory factor TNF-a is decreased, while that of the anti-inflammatory cytokine IL-10 is increased at 72 h after ischemia [34]. Therefore, we speculate that transcription factors regulate the levels of aquaporins, TJ proteins and inflammatory cytokines, further inducing a recovery of BBB integrity.…”
Section: Discussionmentioning
confidence: 99%
“…The inflammatory response is also modulated by the autonomic nervous system, physiological activation of sympathetic nervous system is in general pro‐inflammatory, while parasympathetic activity is antiinflammatory (Pongratz & Straub, ; Tracey, ). However, severe conditions, such as stroke or polytrauma may be associated with delayed immunosuppression, possibly due to fact that severe conditions represent very strong stress, which may be associated with overstimulation of sympathetic nervous system and subsequent direct or rebound immunodepression (Jiang, ; Yan & Zhang, ; Zuo, Shi, & Yan, ).…”
Section: Strokementioning
confidence: 99%
“…Cyclic AMP in turn represents the second messengers of many G-protein mediated hormone and cytokine responses [154] (e.g., induction of hepatic glycogenolysis after β-adrenergic stimulation [155]), processes of cell differentiation, cytoskeletal remodeling and proliferation in addition to apoptosis and immune modulation [156]. While AGE formation is thought to be part of pro-inflammatory signaling cascades (via RAGE and NFκB), recent in vivo studies suggest that globally high cAMP concentrations have moderate immunosuppressive effects [157,158]. Furthermore, cAMP-impaired neutrophil chemotaxis in vitro [159] decreased the release of histamine and leukotrienes from basophils or mast cells [160], which significantly reduced ROS formation [161,162].…”
Section: Different Aspects Of the Stress Response In Sepsismentioning
confidence: 99%