Effect of hyperbaric oxygen preconditioning on the expression of HO-1 and ALK in cerebral ischemia-reperfusion rats
- Author:
- No author available
- Journal Title:
- Chinese Journal of Nautical Medicine and Hyperbaric Medicine
- Issue:
- 5
- DOI:
- 10.3760/cma.j.issn.1009-6906.2018.05.007
- Key Word:
- 高压氧预处理;脑缺血再灌注;血红素氧合酶-1;间变性淋巴瘤激酶;大鼠;Hyperbaric oxygen preconditioning;Cerebral ischemia-reperfusion;Heme oxygenase-1;Anaplastic lymphoma kinase;Rat
Abstract： Objective To study the effects of hyperbaric oxygen ( HBO ) preconditioning on the expression of heme oxygenase-1 ( HO-1 ) and anaplastic lymphoma kinase ( ALK ) in cerebral ischemia-reperfusion ( IR) rats.Methods The Sprague-Dawley male rats were randomly divided into 3 groups: the middle cerebral artery occlusion (MCAO) and reperfusion group (n=8), the sham surgical group (n=7) and the HBO preconditioning +MCAO and reperfusion group (n=8).The HBO preconditioning rats were exposed to hyperbaric environment at a pressure of 0.2 MPa with 85％ oxygen concentration , 1 hour a day, for a succession of 7 days.Modified Longa method was used to develop middle cerebral artery occlusion ( MCAO) model and reperfusion was performed 2 hours after ischemia .Twenty-fours after termination of reperfusion , the samples were collected to perform TTC staining , and RT-PCR was used to detect the expression levels of HO-1 and ALK.Results HBO preconditioning could significantly reduce the scope of cerebral infarction ( P <0.01).Additionally, the expression levels of HO-1 and ALK in the ischemia and reperfusion group were markedly increased , as compared with those of the sham surgical group , while the expression levels of HO-1 and ALK in the HBO group were considerably decreased , however , the expression level of HO-1 was obviously increased as compared with that of the sham surgical group (P<0.05).Conclusion HBO preconditioning could significantly decrease the down-regulation of HO-1 and ALK in the brain tissue of ischemia and reperfusion rats , which indicated that it might have a protective effect on the brain damage induced by ischemia and reperfusion .
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