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. 2011 Nov;17(11):BR299-304.
doi: 10.12659/msm.882038.

Remote ischemic preconditioning protects neurocognitive function of rats following cerebral hypoperfusion

Tao Xu  1 , Zheng Gong, Wen-zhong Zhu, Jia-feng Wang, Bo Li, Feng Chen, Xiao-ming Deng
Affiliations

Remote ischemic preconditioning protects neurocognitive function of rats following cerebral hypoperfusion

Tao Xu et al. Med Sci Monit. 2011 Nov.

Abstract

Background: Protection of remote ischemic preconditioning on neurocognitive function caused by bilateral common carotid artery occlusion has been investigated in rats.

Material/methods: Thirty-six male Sprague-Dawley rats were divided into 3 groups - control group (Group C, n=12), bilateral carotid arteries occlusion group (Group B, n=12) and remote ischemic precondition group (Group P, n=12). In Group P, remote ischemic preconditioning (RIPC) was performed on the right femoral artery with 3 cycles (10 min) of occlusion/perfusion. After 3 cycles of preconditioning, bilateral carotid arteries were occluded immediately for 60 min. In Group B, ischemic insults were conducted without RIPC. Sham surgeries were performed in Group C. Evaluation of memory and learning capacity was performed on days 5-8 after surgery by Morris water maze testing of spatial learning capacity (n=6 for each group). Apoptosis of cells in the hippocampus region was determined by TUNEL tests and Bcl-2 at this region was determined by ELISA 24 h and 9 days after vessel occlusion (n=6 for each group).

Results: Neurocognitive tests showed that latency time was significantly longer in Group B than in Group P on day 7 (p=0.016) and day 8 (p=0.036). Moreover, frequency of platform crossings was significant less in group B than in the other 2 groups on day 9. Bcl-2 level was significantly increased in the hippocampal region of rats in Group P on days 1 and 9 after vessel occlusion. TUNEL test showed that apoptosis could be observed at 24 h after occlusion in Group B, but not in Group P and Group C. No apoptosis was observed on day 9.

Conclusions: Our results suggest that RIPC can protect neurocognitive function of rats after bilateral carotid occlusions, and that Bcl-2 may play an important role in this protective effect.

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Figures

Figure 1
Figure 1
Latency time of Morris water maze. Latency time in each group was not significantly different on day 5 and day 6. But it was significantly different on day 7 (p=0.016) and day 8 (p=0.036) between Group B and Group P, and on day 8 (p=0.047) between Group B and Group C. There were no significantly difference between Group C and Group P in any of the four testing days. * p<0.05 vs. Group B.
Figure 2
Figure 2
Platform crossings of Morris water maze. There was significant difference between Group B and the other 2 groups in frequency of platform crossings on day 9. * p<0.05 vs. Group B
Figure 3
Figure 3
TUNEL assay in hippocampal CA1 region at 24 h after vessel occlusion.
Figure 4
Figure 4
TUNEL assay in hippocampal CA1 region at Day 9 after vessel occlusion.
Figure 5
Figure 5
Enzyme-linked immunoassay (ELISA) of Bcl-2 in hippocampal region of rats. ELISA results demonstrated that Bcl-2 levels were significantly increased in Group P. The levels of Bcl-2 was 2.45±0.53 ng/mg in Group B, 3.15±0.65 ng/mg in Group C and 4.09±0.61 ng/mg in Group P, respectively. Bcl-2 level in Group P was significantly higher than in Group B (p<0.001) and in Group C (p=0.017).There was no significant difference between Bcl-2 levels in Group B and Group C (p=0.063). * p<0.05 vs. Group P.
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