Abstract
Objective To investigate the effect of cerebral ischemic preconditioning （IP） on the expressions of angiopoietin-1 （Ang-1） and its receptor Tie-2 mRNA in cerebral ischemia in rats. Methods Ninety-nine Wistar rats were randomly assigned to three groups： sham operation （n = 9）, non-ischemic preconditioning （NIP） （n =45）, and IP （n =45）. The latter two groups were redivided into 5 subgroups： ischemia-reperfusion 1, 3, 7, 14, and 21 days （n =9 in each group）. A model of transient middle cerebral artery occlusion （MCAO） was induced by the intraluminal suture method for focal IP （ischemia for 10 minutes and restoring perfusion）. Infarct volume was determined by 2,3,5-triphenyltetrazolium staining. The expression levels of Ang-1/Tie-2 mRNA were detected by in situ hybridization. Results The infarct volumes in the 1-, 3-, and 7-day subgroups of the IP group were significantly smaller than those in the relative subgroups of the NIP group （all P 〈 0. 05）. The expression of Ang-1 mRNA in the 3- and 7-day subgroups of the IP group and the expression of Tie-2 mRNA in the 1-, 3-, and 7-day subgroups of the NIP group were upregulated significantly （all P 〈0. 05）. The infarct volume in the 3-day subgroup of the IP group was reduced most significantly （P 〈 0. 05）. The expression of Ang-1 mRNA in the 7-day subgroup was upregulated significantly, and the peak expression of its receptor Tie-2 mRNA appeared at day 3 after IP and continued to day 7. Pearson correlation analysis showed that the expression levels of Ang-1/Tie-2 mRNA were significantly negatively correlated with infarct volume （P 〈 0. 01）. Conelusiom The expression of Ang-1/Tie-2 mRNA in the IP group was upregulated within the time window of ischemic tolerance （1 - 7 days after preconditioning）, in which Ang-1 may mainly act on the later stage of the cerebral ischemic tolerance. Key words: Angiopoietin-1; Receptor, TIE-2; Brain Ischemia; Isch~xrfic Preconditioning In Situ Hybridiza-tion; Time Factors; Disease Models, Animal; Rats
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