Effect of hyperbaric oxygen preconditioning on expression of neuroplasticity after acute global cerebral ischemia-reperfusion in aged rats / 重庆医学

ABSTRACT

Objective To investigate the effect of hyperbaric oxygen preconditioning (HOP)on expression of Nogo mRNA,No-go-A and Ng R protein in the cerebral cortex after acute global cerebral ischemia-reperfusion (I/R)in aged rats and to study its mechanism affecting neuroplasticity.Methods Forty-two aged male SD rats were randomly divided into 4 groups:control group (C group,n=6),hyperbaric oxygen group (H group,n=12),cerebral I/R injury group (I/R group,n=12)and HOP group (n=12). The H group and the HOP group were placed in the hyperbaric oxygen cabin for 1 h per day with a oxygen pressure of 0.2 Mpa for successive 5 d,at 24 h after last time of hyperbaric oxygen preconditioning the I/R group and the HOP group adopted the modified Pulsinelli vessel occlusion method for preparing the rat I/R injury model,with global cerebral ischemia for 10 min and reperfusion for 24 h,each 6 rats were randomly taken from the the H group,I/R group and HOP group and their heads were cut off for taking the brain and isolating the cerebral cortex.The real time fluorescence quantification PCR was adopted to detect the expression level of Nogo mRNA and the Nogo-A protein level was detected by Western blot.The rats in various groups were performed the T1 WI and T2WI scanning in the transection position and the coronal positions.Results There were no obvious ischemic brain infarction in the normal control group and the H group,the arc-shaped bilateral cortex ischemic infarct area was clearly seen in the ischemic group,the ischemic infarct area was also seen in the HOP ischemia group,but its area was smaller than which in the ischemic group.Compared with the C group,the expression of Nogo mRNA and the Nogo-A protein in the HOP group was up-regulated(P<0.05);compared with the I/R group,the expression of Nogo mRNA and the Nogo-A protein was down-regulated(P<0.05). Conclusion HOP increases the neuroplasticity and can reduce the cerebral ischemic infarction area in the exceed acute stage of rat acute global cerebral ischemia by inhibiting Nogo mRNA in the cerebral cortex and up-regulating the Nogo-A protein expression.