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目的探讨载脂蛋白E(apolipoprotein E,apoE)与蛛网膜下腔出血(subarachnoid hemorrhage,SAH)后脑组织中内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)表达的关系。方法采用枕大池注血法构建小鼠蛛网膜下腔出血模型。将30只apoE基因敲除(apoE knock out,apoE KO)鼠和30只apoE基因野生(apoE wild type,apoE WT)鼠均随机抽签分为对照组、蛛血组、干预组,每组10只;对照组为枕大池注射40μL的生理盐水,蛛血组为枕大池注射40μL自体尾动脉血,干预组在枕大池注血前6周,每天胃内灌注促进apoE蛋白表达的肝X受体激动剂T0901317 10 mg/(kg.d);RT-PCR和Western blot法分别检测术后12 h各组脑组织中eNOS的mRNA和蛋白表达情况。结果对照组apoE KO鼠及apoE WT鼠eNOS mRNA[(0.823±0.015)vs(0.811±0.021)]和蛋白[(0.902±0.038)vs(0.875±0.041)]之间的表达无明显差异(P>0.05);与对照组相比,蛛血组eNOS mRNA和蛋白表达明显降低,且蛛血组内apoE KO鼠eNOSmRNA[(0.411±0.022)vs(0.613±0.036)]和蛋白[(0.578±0.061)vs(0.694±0.026)]表达较apoE WT鼠更降低(P<0.05);与apoE WT蛛血组相比,apoE WT干预组eNOS的mRNA(0.796±0.052)和蛋白(0.775±0.062)表达明显增加(P<0.05),但apoE KO干预组eNOS的表达与apoE KO蛛血组相比无明显差异(P>0.05)。结论 apoE与SAH后脑组织中eNOS的表达有关;增加脑组织中apoE的表达能明显促进eNOS的表达增加。
Objective To investigate the relationship between the expression of endothelial nitric oxide synthase (eNOS) and brain tissue after apolipoprotein E (apoE) and subarachnoid hemorrhage (SAH). Methods The subarachnoid hemorrhage model was established by occipital cistern injection. Thirty 30 apoE knockout (apoE knockout) and 30 apoE wild type (apoE WT) mice were randomized into control group, spleen group and intervention group, with 10 . The control group was injected with 40μL of physiological saline into the cisterna magna, and 40μL autologous caudal arterial blood was injected into the cisterna magna. In the intervention group, 6 weeks before the injection of occipital cisterna, intragastric infusion of apoE protein T0901317 10 mg / (kg.d). The mRNA and protein expression of eNOS in each group were detected by RT-PCR and Western blot respectively 12 h after operation. Results There was no significant difference in the expression of eNOS mRNA in the apoE KO and apoE WT mice between the control group [(0.823 ± 0.015) vs (0.811 ± 0.021)] and the protein [(0.902 ± 0.038) vs (0.875 ± 0.041)], 0.05). Compared with the control group, the expression of eNOS mRNA and protein in the spleen blood group was significantly decreased, and the eNOS mRNA in the apoE KO mice [(0.411 ± 0.022) vs (0.613 ± 0.036) vs protein [(0.578 ± 0.061) (0.694 ± 0.026)] in apoE WT group was significantly lower than that in apoE WT group (P <0.05). Compared with the apoE WT group, the expression of eNOS mRNA (0.796 ± 0.052) and protein (0.775 ± 0.062) (P <0.05). However, the expression of eNOS in apoE KO intervention group was not significantly different from that in apoE KO spleen blood group (P> 0.05). Conclusions ApoE is related to the expression of eNOS in brain tissue after SAH. Increasing the expression of apoE in brain tissue can obviously promote the expression of eNOS.