Objective: The purpose of this study is to observe neuroprotective effects of hypoxia preconditioning（HP）in
primary culture newborn SD rat hippocampus neurons and 3-n-butylphalide（NBP) against oxygen glucose deprivation/
reoxygenation (OGD/R) injury, and investigate the possible mechanisms against ischemic reperfusion injury. Methods:
After 7-days culture, the hippocampal neurons were initially divided into three groups: normal control group, simple
hypoxia group and HP group. Later, we established OGD30min/R8h model. So, the hippocampal neurons were eventually
divided into five groups: normal control group, OGD/R model group, OGD/R+3-n-butylphalide (NBP)
groups（0.1μmol/L, 1μmol/L and 10μmol/L). Bcl-2 and neuroglobin (NGB) expression of cells in each group were analyzed
by immunocytochemistry. The mRNA expression of Bcl-2 and NGB in each group was analyzed by RT-PCR. Results:
The results showed that the protein and mRNA levels of Bcl-2 and NGB were significantly increased in the HP
group compared to the hypoxia group (P < 0.01). In the OGD/R model, NBP groups also showed a significantly increased
expression of proteins Bcl-2 and NGB compared to the OGD/R (P < 0.05); Different concentration of NBP drugs showed
a significantly increased expression of proteins Bcl-2 and NGB with the increase in NBP concentration (P < 0.01). Conclusion:
The neuroprotection of HP and NBP may share the same possible mechanisms and have endogenous neuroprotection
by up regulating the mRNA and protein expression of Bcl-2 and NGB.
Keywords: 3-N-butylphalide, Bcl-2, hippocampal neurons, HP, neuroglobin, OGD/R.
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