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目的:观察红景天甙对间歇性低压低氧诱导的载脂蛋白E基因敲除(ApoE-/-)小鼠动脉粥样硬化斑块稳定性的影响。方法:30只8周龄健康雄性ApoE-/-小鼠随机分为常压常氧组(对照组)、间歇性低压低氧组(低压低氧组)、低压低氧+红景天甙组(干预组),其中低压低氧组和干预组被放置在模拟海拔5 000m低压低氧舱内每天8h,每组给予相同的普通饮食喂养,干预组灌服红景天甙30mg·kg-1·d-1,而对照组和低压低氧组灌服等量蒸馏水。连续灌胃12周后取小鼠血样测空腹血糖及血脂,取小鼠主动脉根部的主动脉,Masson染色观察动脉粥样硬化斑块的大小及斑块内的胶原纤维含量,免疫组织化学染色检测基质金属蛋白酶-2(MMP-2)、基质金属蛋白酶-9(MMP-9)及基质金属蛋白酶组织抑制剂-2(TIMP-2)蛋白的表达情况。结果:3组空腹血糖和血脂水平差异无统计学意义;与对照组比较,低压低氧组的动脉粥样硬化斑块面积明显增加,胶原含量明显减少(均P<0.01);与低压低氧组比较,红景天甙干预组斑块面积及MMP-2、MMP-9蛋白水平明显降低,而斑块胶原含量及TIMP-2蛋白水平明显增加(均P<0.01)。结论:红景天甙能抑制间歇性低压低氧诱导的动脉粥样硬化斑块形成,并提高斑块的稳定性,其机制可能与红景天甙增加斑块内胶原含量和降低MMP-2、MMP-9,提高TIMP-2蛋白的表达有关。
Objective: To observe the effect of salidroside on the atherosclerotic plaque stability induced by intermittent hypobaric hypoxia in apolipoprotein E gene knockout (ApoE - / -) mice. Methods: Thirty healthy 8-week old male ApoE - / - mice were randomly divided into normoxia group (control group), intermittent hypobaric hypoxia group (hypobaric hypoxia group), hypobaric hypoxia group + salidroside group (Intervention group). The hypoxia-hypoxia group and the intervention group were placed in simulated low altitude hypoxia chamber at 5 000 m altitude for 8 h everyday. Each group was fed with the same general diet. The intervention group was given salidroside 30 mg · kg -1 · D-1, while the control group and hypobaric hypoxia group were given the same amount of distilled water. After 12 weeks of continuous gavage, the fasting blood glucose and blood lipids were taken from the blood samples of mice and the aorta in the aortic root of mice was taken. The size of atherosclerotic plaque and the content of collagen fibers in plaque were observed by Masson staining. Immunohistochemical staining The expressions of MMP-2, MMP-9 and TIMP-2 were detected. Results: Compared with the control group, the area of atherosclerotic plaque in hypobaric hypoxia group increased significantly and the content of collagen decreased significantly (all P <0.01). Compared with low pressure hypoxia group Compared with the control group, plaque area and MMP-2, MMP-9 protein levels were significantly decreased in the salidroside intervention group, while plaque collagen content and TIMP-2 protein levels were significantly increased (all P <0.01). Conclusions: Salidroside can inhibit the formation of atherosclerotic plaque induced by intermittent hypobaric hypoxia and improve the plaque stability. The mechanism may be related to the increase of plaque collagen content and the decrease of MMP-2 , MMP-9, increase the expression of TIMP-2 protein.