2016
DOI: 10.14336/ad.2015.1123
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Abstract: Transient forebrain ischemia induces delayed death of the hippocampal pyramidal neurons, particularly in the CA2 and medial CA1 area. Early pharmacological inhibition of inflammatory response can ameliorate neuronal death, but it also inhibits processes leading to tissue regeneration. Therefore, research efforts are now directed to modulation of post-ischemic inflammation, with the aim to promote beneficial effects of inflammation and limit adverse effects. Transcription factor NF-κB plays a key role in the in… Show more

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Cited by 14 publications
(7 citation statements)
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“…Indeed, NFkB has been shown to drive the expression of iNOS (Marks-Konczalik et al, 1998;Ozawa et al, 2004). In addition, p38 has been shown to be able to activate NFkB (Madrid et al, 2001) and concomitantly, inhibition of p38 and NFkB signaling is beneficial in ischemic stroke (Koistinaho et al, 2002;Nurmi et al, 2004;Zhao et al, 2017;Rolova et al, 2016).…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, NFkB has been shown to drive the expression of iNOS (Marks-Konczalik et al, 1998;Ozawa et al, 2004). In addition, p38 has been shown to be able to activate NFkB (Madrid et al, 2001) and concomitantly, inhibition of p38 and NFkB signaling is beneficial in ischemic stroke (Koistinaho et al, 2002;Nurmi et al, 2004;Zhao et al, 2017;Rolova et al, 2016).…”
Section: Discussionmentioning
confidence: 99%
“…Nfkb regulates the expression of inflammatory cytokines, chemokines, adhesion molecules, and apoptosis of several cell types ( Karin and Lin, 2002 ; Bourteele et al, 2007 ). Since deletion of Nfkb1 can decrease the inflammatory response to brain injury ( Rolova et al, 2015 ) and age-related brain inflammation is linked to augmented Nfkb1 expression ( Primiani et al, 2014 ), it is possible that the enhanced expression of Nkfb1 plays a role in the persistent inflammation observed in the hippocampus of GWI-rats. It could also be the reason for the enhanced expression of other pro-inflammatory cytokine genes such as Bcl6, Csf2, IL1a, and IL6.…”
Section: Discussionmentioning
confidence: 99%
“…Tissue sections were deparaffinized and washed in 0.1 M sodium phosphate buffered saline (PBS) [20], then processed with 3% H 2 O 2 , incubated in 1% BSA for 1 hour and incubated with primary antibodies anti-Brn3a (1:100, Santa Cruz Biotechnology, CA) and anti-glial fibrillary acidic protein (GFAP, 1:100, Santa Cruz Biotechnology, CA) at 4°C overnight. After washing with PBS, sections were incubated with the appropriate secondary antibodies for 1 hour at room temperature.…”
Section: Methodsmentioning
confidence: 99%