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目的 :观察有氧运动对ApoE基因缺陷小鼠动脉粥样硬化 (AS)斑块形成、胸主动脉中诱导型NOS(iNOS)和内皮型NOS(eNOS)蛋白含量及血清NO浓度的影响 ,以期探讨有氧运动调节血脂代谢以外的抗AS机制。方法 :10周游泳运动后 ,测定ApoE基因缺陷小鼠AS斑块面积和血清NO浓度。采用免疫组织化学染色及计算机模拟图像定量分析法测定胸主动脉iNOS和eNOS的蛋白含量。常规HE染色和胸主动脉矢状面油红 -O大体染色观察。结果 :运动组ApoE基因缺陷小鼠AS斑块平均面积小于对照组 (P <0 0 1) ,NO浓度和eNOS蛋白含量显著高于对照组 (P <0 0 1) ,胸主动脉iNOS蛋白含量显著低于对照组 (P <0 0 5 ) ,血管壁及内膜损伤程度较对照组轻。结论 :有氧运动可能通过增高eNOS蛋白 ,抑制iNOS蛋白 ,提高生物活性形式的NO浓度 ,以改善血管内皮功能 ,延缓动脉粥样硬化斑块的发生发展 ,这可能属独立于血脂调节作用以外的其他抗动脉粥样硬化机制。
Objective: To observe the effect of aerobic exercise on the formation of atherosclerotic plaque in ApoE-deficient mice, the content of inducible NOS (iNOS) and endothelial nitric oxide synthase (eNOS) and the concentration of serum NO in the thoracic aorta, Discussion Aerobic exercise regulates anti-AS mechanism other than lipid metabolism. Methods: After 10 weeks of swimming, the area of AS plaque and serum NO in ApoE gene-deficient mice were measured. The protein content of iNOS and eNOS in the thoracic aorta was determined by immunohistochemical staining and computerized image quantitative analysis. Routine HE staining and sagittal oily red-O gross staining of the thoracic aorta were observed. Results: The mean plaque area of ApoE gene-deficient mice in exercise group was smaller than that in control group (P <0.01), NO concentration and eNOS protein content were significantly higher in control group (P <0.01), and the content of iNOS protein in thoracic aorta Significantly lower than the control group (P <0 05), the degree of vascular wall and endometrial damage than the control group. CONCLUSION: Aerobic exercise may improve vascular endothelial function and delay the development of atherosclerotic plaque by increasing eNOS protein, inhibiting iNOS protein and increasing the concentration of NO in bioactive form, which may be independent of the regulation of blood lipid Other anti-atherosclerotic mechanisms.