Objective      To explore the association between apolipoprotein E (apoE) and cerebral endothelial nitric oxide synthase (eNOS) after subarachnoid hemorrhage (SAH).       Methods      Thirty apoE knock-out (apoE KO) mice and 30 apoE wild type (apoE WT) mice were randomly and equally divided into 3 groups

control

SAH group and intervention group. Mouse model of SAH were inflicted with injecting 40 μL autologous fresh blood taken from tail arterial blood into magna cysterna

while control group with only normal saline. Intervention group was preconditioned by orally taking of liver X receptor (LXR) agonist T0901317 at dose of 10 mg/(kg·d) in 6 weeks before operation. Expression of eNOS at mRNA and protein levels was detected in the brain tissue by RT-PCR and Western blotting respectively.       Results      There was no significant difference in expression of eNOS mRNA and protein in the control groups of apoE KO and WT mice (mRNA: 0.823±0.015 vs 0.811±0.021; protein: 0.902±0.038 vs 0.875±0.041

P0.05). Compared with the control groups

the expression of eNOS at mRNA and protein levels was significantly reduced in SAH groups nor matter of KO or WT mice (P0.05)

and more significant reduce was found in apoE KO mice (mRNA: 0.411±0.022 vs 0.613±0.036

protein: 0.578±0.061 vs 0.694±0.026

P0.05). The expression of eNOS at mRNA and protein levels was significantly higher in apoE WT intervention group than apoE WT SAH group (mRNA: 0.796±0.052 vs 0.613±0.036

protein: 0.775±0.062 vs 0.694±0.026

P0.05)

but there was no significant difference between apoE KO intervention group and apoE KO SAH group (P0.05).       Conclusion      apoE is involved in the expression of cerebral eNOS after SAH. Enhancing cerebral apoE expression significantly promotes the expression of eNOS and thus leads to alleviate cerebral vasospasm after SAH.