| With the deepening of the medical research and development on the mechanism of cerebral ischemia and injury mechanism of the understanding and exploring continuously expand and deepen in recent years. The study of brain ischemic preconditioning(BIP) on brain protection is the focus of attention at home and abroad. The findings of brain protection mechanisms to improve nerve tissue of cerebral ischemic injury tolerance provide a new strategy for prevention and control of hypoxic ischemia encephalopathy. Ischemic tolerance(IT) refers to the adaptive response to transient ischemia and reperfusion, which can improve tissue tolerance during the following damage caused by more severe ischemic events[1]. This phenomenon showed strong endogenous neural protection mechanism, but the detailed mechanism has not been fully elucidated. The objective of this article is to study the changes of nuclear factor-κB(NF-κB), Hairy enhancer of split homologues(Hes1) and B-cell lymphoma/Ieukemia-2(Bcl-2) in hippocampus reperfusion after cerebral ischemia, investigate the neuroprotection of IT and its mechanism.Take 108 healthy male SD rats of clean grade and use digital method to divide them into ischemia/reperfusion(IR) group, ischemia preconditioning(IP) group and the sham operation group randomly, with 36 rats in each group. The IR group was set up by the way of middle cerebral artery occlusion(MCAO)[2]. IP group: The right internal carotid artery was blocked transiently 10 minutes at a time. After 3 days, use the middle cerebral artery occlusion to establish focal cerebral ischemic reperfusion injury model. The sham group only isolated carotid artery. Divide them into 1,2,3,7,14 d groups according to five observation points. Evaluating the neural behavior of rats by the way of Zea-Longa, detecting the volume of cerebral infarctionby the way of 2, 3, 5-Triphenyltetrazolium Chloride(TTC) solution, implementing the real-time fluorescence quantitative polymerase chain reaction(q RT-PCR) method to detect the m RNA expression of NF-κB、Hes1 and Bcl-2.Compared with sham operation group, the differences of neural function defect score and volumes cerebral of rat in IR and IP group were statistical significant(P<0.05); Difference between the IR and IP groups was significant(P<0.05). Compared each group at the same time point: The expression of NF-κB m RNA in IR group and IP group were higher than that in the sham operation group, IP group was lower than that in IR group(P<0.05); The expression of Hes1 m RNA of IR group and IP group were higher than that in the sham operation group, IP group was higher than that in the IR group(P<0.05); The Bcl-2 m RNA expression, compared with sham operation group, IP group reperfusion expressed significantly higher, and higher than that of IR group in 1 and 2 days, the difference was statistically(P<0.05), between each groups there have no statistical in 3, 7, 14 days(P>0.05). Above results suggest that: Negative regulation of Hes1 、Bcl-2 and positive regulation of NF-κB after ischemic preconditioning may be an important molecular mechanism of endogenous nerve regeneration, play a important role in the brain protection. |
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