2013
DOI: 10.1016/j.bbi.2012.12.016
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Preconditioning to mild oxidative stress mediates astroglial neuroprotection in an IL-10-dependent manner

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Cited by 32 publications
(14 citation statements)
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“…Further, we observed an increase in the anti-inflammatory cytokine IL-10 before asphyxia. IL-10 can reduce hypoxia-induced hyperexcitability in hippocampal slice neurons [38], and is an essential mediator of astroglial pre-conditioning to mild oxidative stress in culture [39]. Sevoflurane-induced postconditioning of global cerebral ischemia in adult rats is associated with suppression of pro-inflammatory cytokines and increased IL-10 [40].…”
Section: Discussionmentioning
confidence: 99%
“…Further, we observed an increase in the anti-inflammatory cytokine IL-10 before asphyxia. IL-10 can reduce hypoxia-induced hyperexcitability in hippocampal slice neurons [38], and is an essential mediator of astroglial pre-conditioning to mild oxidative stress in culture [39]. Sevoflurane-induced postconditioning of global cerebral ischemia in adult rats is associated with suppression of pro-inflammatory cytokines and increased IL-10 [40].…”
Section: Discussionmentioning
confidence: 99%
“…The transcription factor Nrf2 is expressed widely throughout the body and upregulates the expression of numerous antioxidant genes in response to oxidative stress (88, 89). In astroglia preconditioned to oxidative stress, neuroprotection from oxidative stress–glucose deprivation was reported to be via an Nrf2/IL-10-dependent mechanism (90). Lipocalin-2 is significantly increased in neurons following stroke and is proposed to signal stress from injured neurons to supporting glia (91).…”
Section: Ischemic Strokementioning
confidence: 99%
“…Such stimulatory responses reflect either a direct stimulation or an overcompensatory effect, and occur independently of biological model, cell type, inducing agent, and mechanism (Calabrese, 2011, ). Hormetic effects are currently being ever more considered for biomedically therapeutic applications (Calabrese, ) in that these responses appear to be involved in a number of developmental, maturational, and aging processes (Calabrese et al, ; Segev‐Amzaleg, Trudler, & Frenkel, ), and may subserve a spectrum of activities in neural systems, including protection against and/or recovery from certain neurodegenerative diseases, and/or injury (Calabrese, ). The iterative recognition of hormesis has occurred in large part because traditional dose–response constructs, such as the threshold model, have not been able to satisfactorily and/or fully account for nonrandom biological activity below well‐established thresholds of response.…”
Section: Hormesis: Background and Perspectivesmentioning
confidence: 99%