Effects of isoflurane preconditioning on expression of TLR4 and MyD88 during focal cerebral ischemiareperfusion in rats
10.3760/cma.j.issn.0254-1416.2010.09.025
- VernacularTitle:异氟醚预处理对大鼠局灶性脑缺血再灌注时TLR4和MyD88表达的影响
- Author:
Zhibin XIAO
;
Changjun GAO
;
Xiaoxu TANG
;
Zhen ZHANG
;
Jun WANG
;
Yuming ZHANG
;
Wei CHAI
;
Xude SUN
- Publication Type:Journal Article
- Keywords:
Isoflurane;
Ischemic preconditioning;
Toll-like receptor 4;
Myeloid differentiation factor 88;
Reperfusion injury;
Brain
- From:
Chinese Journal of Anesthesiology
2010;30(9):1102-1104
- CountryChina
- Language:Chinese
-
Abstract:
Objectiye To investgate the effects of isoflurane preconditioning on expression of Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) during focal cerebral ischemia-reperfusion (IR) in rats. Methods Thirty male SD rats weighing 250-300 g were randomly divided into 3 groups ( n = 10 each):sham operation group (group S);focal cerebral IR group and isoflurane preconditioning group (group IP). The animals were anesthetized with intraperitoneal pentobarbital 40 mg/kg. In group IR and IP a nylon thread with rounded tip was inserted into right internal jugular vein and threaded cranially until resistance was met. Mid-cerebral artery was occluded (MCAO) for 2 h followed by 24 h reperfusion. In group IP the animals inhaled 2% isoflurane98 % O2 for 1 h once a day for 5 consecutive days at 24 h before MCAO. Neurologic function was assessed and scored and cerebral infarct volume was measured at 24 h of reperfusion. The animals were sacrificed at 24, 48 and 72 h of reperfusion respectively. The right ischemic frontal lobes were removed for determination of TLR4, MyD88and NF-κB expression by Western blot analysis. Results MCAO significantly worsened neurologic function. The neurologic function deficit scores were significantly increased and the TLR4, MyD88 and NF-κB expression were significantly up-regulated in group IR as compared with group S (P ＜ 0.05). Isoflurane preconditioning significantly decreased cerebral infarct volumes and neurologic function deficit scores and down-regulated the expression of TLR4, MyD88 and NF-κB in group IP as compared with group IR ( P ＜ 0.05). Conclusion Isoflurane preconditioning can reduce inflammatory response and focal cerebral IR injury by down-regulating the expression of TLR4and Myd88.
