CAJ | 학술논문

目的探讨家兔动脉粥样硬化及斑块形成与血小板源内皮型氧化氮合酶(eNOS)表达的关系. 方法设立模型组、治疗组和非治疗组及对照组,每组家兔6只.模型组、治疗组和非治疗组每天给予胆固醇饮食,至12周建立家兔动脉粥样硬化模型,建模后继续喂养至24周,同时治疗组服用普伐他汀10 mg/d;非治疗组仅给予普通饮食.实验终点剥离家兔主动脉观察大体和组织病理形态,反转录一聚合酶链式反应(RT-PCR)方法检测血小板源eNOS/mRNA水平. 结果模型组和非治疗组均可见明显动脉粥样硬化和(或)斑块形成;主动脉最大脂纹或斑块厚度占整个血管壁厚度的百分比,对照组、模型组、治疗组和非治疗组分别是0.04±0.02、0.82±0.16、0.33±0.18和0.77±0.14,治疗组与非治疗组比较,差异有统计学意义(F=33.759,P=0.001).血小板(2～4×108/ml)eNOS mRNA表达在对照组、模型组、治疗组和非治疗组分别是1.02±0.28、0.41±0.27、1.00±0.77、0.40±0.29,治疗组较非治疗组明显增高(F=3.544,P=0.02). 结论血小板源eNOS表达与动脉粥样硬化及斑块的形成呈负相关;普伐他汀对动脉粥样硬化及斑块的逆转作用可能与血小板源eNOS有关.
목적 탐토가토동맥죽양경화급반괴형성여혈소판원내피형양화담합매(eNOS)표체적관계. 방법 설립모형조、치료조화비치료조급대조조,매조가토6지.모형조、치료조화비치료조매천급여담고순음식,지12주건립가토동맥죽양경화모형,건모후계속위양지24주,동시치료조복용보벌타정10 mg/d;비치료조부급여보통음식.실험종점박리가토주동맥관찰대체화조직병리형태,반전록일취합매련식반응(RT-PCR)방법 검측혈소판원eNOS/mRNA수평. 결과 모형조화비치료조균가견명현동맥죽양경화화(혹)반괴형성;주동맥최대지문혹반괴후도점정개혈관벽후도적백분비,대조조、모형조、치료조화비치료조분별시0.04±0.02、0.82±0.16、0.33±0.18화0.77±0.14,치료조여비치료조비교,차이유통계학의의(F=33.759,P=0.001).혈소판(2～4×108/ml)eNOS mRNA표체재대조조、모형조、치료조화비치료조분별시1.02±0.28、0.41±0.27、1.00±0.77、0.40±0.29,치료조교비치료조명현증고(F=3.544,P=0.02). 결론 혈소판원eNOS표체여동맥죽양경화급반괴적형성정부상관;보벌타정대동맥죽양경화급반괴적역전작용가능여혈소판원eNOS유관.
Objective To explore the correlation of atheroselerosis progression and the expression of platelet derived endothelial nitric oxide synthase (eNOS) in rabbits. Methods A total of 24 male New Zealand white rabbits were used in this study. Six of the animals were fed with normal food (control group). Eighteen rabbits were fed with cholesterol-rich food (1 g/d) for 12 weeks to establish the atherosclerosis model. Among 18 models, 6 rabbits were executed immediately and their aorta and platelet samples were collected for further analysis (model group), 6 rabbits were orally administered with pravastatin (10 rag/d) for additional 12 weeks (treated group), and the remaining 6 rabbits were left untreated until the end of the study (untreated group). The control, treated and untreated animals were then killed, and the aorta and platelet samples were collected for eNOS expression analysis (RT-PCR). Results The aorta samples in model and untreated group exhibited rough intima and a lot of longitudinal fatty streaks, which indicated that atherosclerosis models were established successfully. While in treated group, the degree of atherosclerosis was decreased. The average percent of thickness of fatty streaks or atheroselerotic plaques relative to the whole thickness of vessel walls was 0. 04±0. 02, 0. 82±0. 16, 0. 33±0. 18,0. 77±0. 14 in control, model, treated and untreated group, respectively. The thickness of fatty streaks or atherosclerotic plaques was significantly increased in the model and untreated groups and decreased in treated group compared with the control group (both P<0. 05). The expressions of platelet derived eNOS/mRNA were 1. 02± 0. 28, 0. 41± 0. 27, 1.00 ± 0. 77, 0. 40±0. 29 in control, model, treated and untreated group, respectively. The expression of eNOS/mRNA was markedly decreased in model group and untreated group compared with the control group, but was increased in treated group compared with untreated and model groups (F=3. 544, P = 0. 024). Conclusions There is a negative correlation between eNOS expression and atherosclerosis development, which suggests that the reversal effect of pravastatin on atheroselerosis progression and plaque formation may relate to the expression of platelet derived eNOS.