Early increases in TNF-α, IL-6 and IL-1β levels following transient cerebral ischemia in gerbil brain☆
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2019, Experimental NeurologyCitation Excerpt :Following cerebral ischemia, an inflammatory response is triggered by activation of microglia and astrocytes with a corresponding upregulation of pro-inflammatory cytokines (Iadecola and Anrather, 2011). In particular, interleukin-1beta (IL-1β) and tumor necrosis factor alpha (TNFα) are pro-inflammatory cytokines that are upregulated within hours following global cerebral ischemia (Saito et al., 1996; Weil et al., 2008) and may remain elevated for weeks (Espinosa-Garcia et al., 2017; Norman et al., 2011), with the potential to exacerbate injury (Fu et al., 2015). The hippocampus is particularly vulnerable to delayed damage following global cerebral ischemia in both animal models (Kirino, 1982) and humans (Horn and Schlote, 1992; Petito et al., 1987).
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2018, Neurochemistry InternationalCitation Excerpt :TNF-α, as a mediator in responding to ischemic injury, is activated in brains of animal models of transient brain ischemia (Murakami et al., 2005; Uno et al., 1997). Saito et al., (1996) reported that TNF-α levels were increased in hippocampus at early phase after TCI in gerbils. Data on time-course changes in TNF-α expression after transient ischemic insults can offer important information about roles of TNF-α in the brain at early stage after transient ischemic insults.
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We appreciate the useful discussion of S.P. Markey, B. J. Quearry, M.P. Heyes and A. Noma.