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目的:探讨有氧运动对小鼠动脉血红素加氧酶-1(heme oxygenase-1,HO-1)的影响及其在抗动脉粥样硬化(atherosclerosis,AS)形成中的作用。方法:采用8周龄C57小鼠和ApoE基因敲除小鼠(ApoE-/-小鼠,饲以高脂饮食饲料建立动脉粥样硬化模型),分为ApoE-/-安静组(AC组)、ApoE-/-运动组(AE组)、C57运动组(CE组)、C57安静组(CC组)4组,每组15只。运动组进行12周中等强度跑台运动(10米/分×30→13米/分×60分,5次/周)。实验12周后安静时取材,采用HE染色、免疫组织化学方法及图像分析系统测定主动脉弓、腹主动脉、颈动脉组织解剖结构及HO-1表达。结果:CC组和CE组动脉组织结构正常。AC组主动脉多为纤维粥样硬化期病变,AE组多为脂纹脂斑早期病变。CC组主动脉无HO-1表达,CE组主动脉内皮层有HO-1表达。AC组主动脉内皮细胞和斑块可检测到HO-1大量表达,AE组比AC组表达减少。经图像分析,和AC组比,AE组主动脉弓、腹主动脉和颈动脉HO-1表达显著下降(分别为P<0.01、P<0.05、P<0.05),其中主动脉弓减少比腹主动脉、颈动脉明显。结论:有氧运动增强正常动脉的抗氧化能力(HO-1表达增加)。运动延缓AS形成中的动脉病变,可能与其降低主动脉的氧化应激水平(氧化应激标志HO-1降低)有关。这些改变均以主动脉弓表现明显。
Objective: To investigate the effect of aerobic exercise on heme oxygenase-1 (HO-1) and its effect on the formation of atherosclerosis (AS). Methods: ApoE - / - quiescent mice (ApoE - / - mice) were divided into ApoE - / - quiescent group (AC group) and C57 mice (8 weeks old) and ApoE knockout mice , ApoE - / - exercise group (AE group), C57 exercise group (CE group) and C57 sedation group (CC group). Exercise group for 12 weeks of moderate treadmill exercise (10 m / min × 30 → 13 m / min × 60 min, 5 times / week). Twelve weeks after the experiment, the animals were taken at a quiet time. The structures of the aortic arch, abdominal aorta and carotid artery and the expression of HO-1 were detected by HE staining, immunohistochemistry and image analysis system. Results: The structure of arteries in CC group and CE group was normal. The aorta in AC group was mostly fibrous atherosclerotic lesion, and the AE group was mostly the early lesion of lipid pattern. In the CC group, there was no HO-1 expression in the aorta and HO-1 expression in the CE group. HO-1 expression was detected in aortic endothelial cells and plaques in AC group, and decreased in AE group compared with AC group. After image analysis, the expression of HO-1 in aortic arch, abdominal aorta and carotid artery of AE group was significantly lower than that of AC group (P <0.01, P <0.05, P <0.05, respectively) Artery obvious. CONCLUSION: Aerobic exercise increases the antioxidant capacity of normal arteries (increased HO-1 expression). Exercise retarding the development of arterial lesions during AS formation may be related to its ability to reduce the level of oxidative stress in the aorta (reduced oxidative stress marker HO-1). These changes are evident in the aortic arch.