Experimental study on the protective effects of ischemic preconditioning on brain ischemia-reperfusion injury in mice
- VernacularTitle:脑缺血预处理对小鼠脑缺血再灌注损伤的保护作用
- Author:
Chaoran WU
;
Jianying ZHAO
;
Chongtian WU
- Publication Type:Journal Article
- Keywords:
Ischemic preconditioning;
Brain;
Reperfusion injury
- From:
Chinese Journal of Anesthesiology
1996;0(09):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To develop a forebrain ischemic preconditioning model in C57BL/6 mice and determine the protective effects of ischemic preconditioning on brain ischemia-reperfusion injury. Methods Forty-eight 8-10 week old C57BL/6 mice weighing 19-23 g were randomly divided into four groups of 12 animals, A: sham-operation group; B: ischemic preconditioning group; C: ischemia-reperfusion group (I/ R); D: ischemic preconditioning + I/R group. The animals were anesthetized with halothane. Bilateral common carotid artery (BCCA) was exposed and occluded for 6min (ischemic preconditioning) or 18min followed by 3h reperfusion (I/R). In group D BCCA was firstly occluded for 6 min, then released and 48h later occluded again for 18min followed by 3h reperfusion. 6 animals in each group were sacrificed 72h after reperfusion and brain was immediately removed for detection of DNA fragmentation of neurons in hippocampus by TUNEL. Another 6 animals were sacrificed on the 7th day after I/R and neuronal damage was identified by microtubule-associated protein-2 immunochemistry and quantified by cresyl violet staining. Results I/R resulted in severe damage to hippocampus in C57BL/6 mice. The ischemic preconditioning caused neither noticeable hippocampal neuronal damage nor DNA fragmentation but significantly reduced hippocampal neuronal damage and DNA fragmentation caused by I/R. Conclusion Our results indicate that hippocampal neuronal injury induced by I/R can be greatly reduced by ischemic preconditioning in C57BL/6 mice. Many kinds of gene-altered C57BL/6 mice are available, this preconditioning model may provide an useful method for investigating the molecular mechanisms of ischemic preconditioning.
