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目的观察运动对动脉粥样硬化(atherosclerosis,AS)形成中主动脉壁超微结构的影响。方法对30只8周龄ApoE基因敲除小鼠(ApoE~(-/-)小鼠)饲以“西方饮食”饲料建立AS模型,30只C57BL/6J小鼠为同源对照鼠,分为C57安静组(CC组,n=15)、C57运动组(CE组,n=15)、ApoE~(-/-)小鼠安静组(AC组,n=15)和ApoE~(-/-)小鼠运动组(AE组,n=15)。两个运动组进行12周中等强度跑台运动,前6周运动量由10m/min×30min渐增为13m/min×60min,后6周以稳定的运动量(13m/min,60min)进行运动,每周5次。12周实验结束后,采用透射电镜观察各组小鼠主动脉内膜、中膜、内皮细胞、平滑肌细胞结构。结果ApoE~(-/-)小鼠安静组动脉壁损伤严重,内皮细胞出现受损、变质、脱落,细胞内连接不紧密。内皮下间隙增宽,内弹力膜破坏和消失。中膜平滑肌结构破坏,合成型平滑肌较多。ApoE~(-/-)小鼠运动组大部内皮细胞的腔面光滑平坦,内皮细胞损害较轻,内皮下仍见泡沫细胞,但层数较AC组少,中膜平滑肌以收缩型为主。结论运动可改善动脉粥样硬化内皮和平滑肌细胞的超微结构改变,减少主动脉的病损,从而发挥抗AS作用。
Objective To observe the effect of exercise on the ultrastructure of aortic wall in the formation of atherosclerosis (AS). Methods Thirty 30-week-old ApoE knockout mice (ApoE ~ (- / -) mice) were fed with “western diet” diet to establish AS model. Thirty C57BL / 6J mice were used as control C57 sedentary group (group C, n = 15), C57 group (n = 15), ApoE ~ (- ) Mouse exercise group (AE group, n = 15). During the first 6 weeks of exercise, the exercise intensity gradually increased from 10m / min × 30min to 13m / min × 60min and then to exercise at a steady exercise amount (13m / min, 60min) 5 times a week. At the end of 12 weeks, the structures of intima, media, endothelial cells and smooth muscle cells of the aorta were observed by transmission electron microscope. Results In the apoE ~ (- / -) mice, the arterial wall of the quiet group was severely damaged, and the endothelial cells were damaged, deteriorated and exfoliated, and the intracellular connections were not tight. Widened under the endothelium, the inner elastic membrane destruction and disappearance. Mesothelium smooth muscle structure damage, synthetic smooth muscle more. Most of endothelial cells in ApoE ~ (- / -) mice exercise group had smooth and flat endothelium with less damage to endothelial cells and foam cells still in the endothelium, but the number of layers was less than that in AC group. . Conclusion Exercise can improve ultrastructural changes of atherosclerosis endothelium and smooth muscle cells, reduce the damage of aorta, and thus play an anti-AS effect.