Mimecan蛋白在血压变异性增加诱导的动脉粥样硬化发展中的作用

发布时间：2018-03-25 13:18

本文选题：mimecan蛋白　切入点：血压变异性　出处：《中南大学学报(医学版)》2017年09期

【摘要】：目的:观察大鼠血压变异性增加诱导的动脉粥样硬化发展中mimecan蛋白的表达变化,以及小鼠胸主动脉平滑肌细胞敲减mimecan蛋白对细胞增殖和迁移的影响。方法:动物实验共分为假手术组和模型组,每组8只。通过大鼠去窦弓神经手术建立血压变异性升高的动物模型,20周后采用检测的血流动力学指标对模型进行验证。胸主动脉进行石蜡切片后,通过免疫组织化学观察血管平滑肌组织的病理学改变及mimecan蛋白的表达变化。原代分离培养小鼠胸主动脉平滑肌细胞。使用小干扰RNA敲减细胞mimecan蛋白,通过5-乙炔基-2'-脱氧尿苷掺入试验观察其对于细胞增殖的改变,通过划痕损伤试验观察其对于细胞迁移的改变。结果:手术20周后,与假手术组相比,模型组大鼠血压变异性参数明显升高,证明模型建立成功。同时,血压变异性增加促进了模型组大鼠胸主动脉中血管平滑肌细胞的增殖与迁移,而mimecan蛋白的表达却显著降低。敲减小鼠血管平滑肌细胞中mimecan蛋白,能显著促进细胞的增殖和迁移。结论:Mimecan蛋白对血压变异性增加诱导的动脉粥样硬化的潜在发展有重要的保护作用,其作用机制可能是通过抑制血管平滑细胞的增殖和迁移而延缓动脉粥样硬化的进程。
[Abstract]:Aim: to observe the expression of mimecan protein in atherosclerosis induced by increased blood pressure variability in rats. And the effect of knockout mimecan protein on proliferation and migration of mouse thoracic aortic smooth muscle cells. Methods: animal experiment was divided into sham operation group and model group. Eight rats in each group were used to establish an animal model with elevated blood pressure variability by denervating sinus arch neurosurgery. The model was verified by measured hemodynamic indexes after 20 weeks. The thoracic aorta was sectioned with paraffin section. The pathological changes of vascular smooth muscle tissue and the expression of mimecan protein were observed by immunohistochemistry. The primary cultured mouse thoracic aortic smooth muscle cells were isolated and cultured. The small interfering RNA knockout cell mimecan protein was used. The changes of cell proliferation and cell migration were observed by the incorporation of 5-acetyl-2-oxy-deoxyuridine. Results: twenty weeks after operation, compared with the sham operation group, the cell migration was observed by scratch injury test. The blood pressure variability parameters in the model group were significantly increased, which proved that the model was established successfully. At the same time, the increased blood pressure variability promoted the proliferation and migration of vascular smooth muscle cells in the thoracic aorta of the model group. However, the expression of mimecan protein decreased significantly. Knockout decreased mimecan protein in vascular smooth muscle cells. Conclusion: Mimecan protein has an important protective effect on the potential development of atherosclerosis induced by increased blood pressure variability. The mechanism may be to delay the progression of atherosclerosis by inhibiting the proliferation and migration of smooth vascular cells.
【作者单位】：济南市第四人民医院心内科;
【基金】：山东省医药卫生科技发展计划(2013ws005)~~
【分类号】：R543.5

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