Effect of isoflurane preconditioning on expression of 5-1ipoxygenase during focal cerebral ischemia-reperfusion in rats
10.3760/cma.j.issn.0254-1416.2012.11.028
- VernacularTitle:异氟醚预处理对大鼠局灶性脑缺血再灌注时5脂氧合酶表达的影响
- Author:
Haigang Lü
;
Pengcheng REN
;
Changjun GAO
;
Meiyan SUN
;
Xiaoyong ZHAO
;
Wei CHAI
;
Xude SUN
- Publication Type:Journal Article
- Keywords:
Arachidonate 5-lipoxygenase;
Isoflurane;
Ischemic preconditioning;
Reperfusion injury;
Brain
- From:
Chinese Journal of Anesthesiology
2012;(11):1383-1386
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of isoflurane preconditioning on the expression of 5-lipoxy-genase (5-LOX) during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty-nine male adult Sprague-Dawley rats weighing 250-300 g were randomly divided into 3 groups (n =13 each):sham operation group (group S); focal cerebral I/R group (group I/R); isoflurane preconditioning group (group Ⅰ).Focal cerebral I/R was produced by mid-cerebral artery occlusion in anesthetized rats.The rats inhaled 2 h of 2％ isoflurane and focal cerebral I/R was produced 24 h later in group I.The neurological deficits were scored at 24 h of reperfusion.The animals were then sacrificed.The brains were immediately removed for determination of the infarct size.The expression of 5-LOX,myeloid differentiation factor88 (MyD88) and nuclear factor kappa B (NF-κB) protein and mRNA was detected using Western blot and RT-PCR respectively.Results Compared with group S,the neurological deficit score was significantly increased,the infarct size was enlarged in groups I/R and I,the expression of 5-LOX,MyD88 and NF-κB protein and mRNA was up-regulated in group I/R,and the expression of 5-LOX mRNA and MyD88 protein and mRNA was up-regulated in group I (P ＜ 0.05).Compared with group I/R,the neurological deficit score was significantly lower,the infarct size was smaller,and the expression of 5-LOX,MyD88 and NF-κB protein and mRNA was lower in group I (P ＜ 0.05).Conclusion Isoflurane preconditioning can reduce focal cerebral I/R injury by down-regulating the expression of 5-LOX and inhibiting MyD88/NF-κB signaling pathway in rats.
