Ischemic postconditioning down-regulates expressions of interleukin- 1β and tumor necrosis factor-α in cerebral ischemia/reperfusion in rats
10.3760/cma.j.issn.1673-4165.2012.02.005
- VernacularTitle:缺血后处理下调脑缺血再灌注大鼠白细胞介素-1β和肿瘤坏死因子-α表达
- Author:
Jinglei LV
;
Guofeng WANG
;
Peng WANG
;
Renliang ZHAO
- Publication Type:Journal Article
- Keywords:
Brain Ischemia;
Ischemic Preconditioning;
Reperfusion Injury;
Interleukin-1β;
Tumor Necrosis Factor-α;
Disease Models,Animal;
Rats
- From:
International Journal of Cerebrovascular Diseases
2012;20(2):135-141
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of ischemic postconditioning (IP) on interleukin-1β (IL-1β) and tunor necrosis factor-α (TNF-α) expression in focal cerebral ischenia/reperfusion in rats in order to clarify the rnechanism of neuroprotective effect of IP.Methods One hundred and ten healthy adult male Sprague-Dawley rats were randomized into sham operation (n =10),ischemia/reperfusion and IP groups.The latter two groups were redivided into 6-,12-,24-,48- and 72-hour subgroups (n =10 in each subgroup) according to their reperfusion time.A focal cerebral ischemia/reperfusion model was induced by the middle cerebral artery intraluminal suture method.After middle cerebral artery occlusion for 2 hours,reperfusion for 15 seconds was conducted using the IP method,and this was repeated for 3 times.The neurobehavioral scores of the rats were evaluated in each group.The infarct volume was measured with 2,3,5-triphenyltetrazolium chloride staining.The expression of TNF-α and IL-1β protein in brain tissue was detected by immunohistochemistry assay.The expression of IL-1β and TNF-αmRNA was determined by in situ hybridization.Results Compared with the ischemia/reperfusion group,the neurobehavioral score and and cerebral infarct volume in the IP group decreased significantly (all P ＜0.05).Expressions of IL-1 β,TNF-o protein and mRNA were slight in the frontoparietal cortex in the sham group; however,they were apparent in ischemia/reperfusion group and IP groups,and began to increase at 6 hours and reached the peak at 24 hours (compared to other time points all P ＜0.05),then decreased gradually.There was the same dynamic change trend in the IP group,and the expression at each time point was significantly lower than that in the ischemia/reperfusion group (all P＜0.05).Conclusions IP significantly down-regulates the expressions of IL-1 β and TNF-α and reduces the infarct volume of the ischemia/reperfusion in rats.These findings indicate that IP may play a neuroprotective role by inhibiting the inflammatory response in brain tissue after ischemia/reperfusion.
