apoE-/-小鼠颈总动脉斑块Fractalkine与TLR4的表达

目的 探讨apoE^-/-小鼠动脉粥样硬化斑块不规则趋化因子fractalkine与Toll样受体4(TLR4)的表达及其关系。方法 24只apoE^-/-小鼠平均分为三组:普通饮食组、高脂饮食组、阿伐他汀干预组。12周后实验结束,检测动物血脂、颈总动脉斑块面积和血管狭窄率,评价AS病变严重程度。最后,应用免疫组织化学方法检测斑块内fractalkine和TLR4的表达情况。结果 高脂饮食组颈总动脉AS斑块面积和血管狭窄率分别是普通饮食组的近4倍和3倍多;而药物干预组二者均降低,但只有血管狭窄率减少有统计学差异(35.27±3.84)vs.(27.02±2.69), P<0.05];斑块处fractalkine、TLR4的表达在高脂饮食组升高(3.24±0.96)vs. (10.69±2.11)、(1.29±0.57) vs (9.32±1.02)],经阿伐他汀干预后表达均下降(10.69±2.11) vs (5.73±1.30)、(9.32±1.02) vs (3.32±0.51),(P<0.05)] 结论 在apoE^-/-小鼠AS斑块内,fractalkine和TLR4呈协同性表达,两者之间可能存在某种分子机制,并在AS的发病过程中发挥重要作用。

Expressions of fractalkine and TLR4 in atherosclerotic plaques in the common carotid artery of apoE-/- mice

Objective To explore the expression and correlation of fractalkine and TLR4 in atherosclerotic plaques in the common carotid artery of apoE^-/- mice. Methods Twenty-four ApoE^-/- mice were divided into three groups, fed with standard chow diet (SD), high-fat diet (HF) or HF and atorvastatin (HF+A).12 weeks later, the blood lipids were checked. The plaque area and vascular stenosis rate of the common carotid artery were measured. All the data were used to evaluate the severity of atherosclerotic lesions of the animals. Moreover, immunohistochemical staining was used to examine the levels of fractalkine and TLR4 expressions. Results The plaque area and vascular stenosis rate of the common carotid artery in the HF group were larger than those in the SD group (about 5-fold and 3-fold), but only vascular stenosis rate of the HF+A group was significantly reduced, compared with the HF group (35.27±3.84 vs. 27.02±2.69, P<0.05). The expressions of fractalkine and TLR4 were significantly increased in the HF group (3.24±0.96 vs. 10.69±2.11, 1.29±0.57 vs. 9.32±1.02), and decreased in the HF+A group (10.69±2.11 vs. 5.73±1.30, 9.32±1.02 vs. 3.32±0.51)(P<0.05). Conclusions The expressions of fractalkine and TLR4 are changed synchronously in apoE^-/- mouse atherosclerotic plaques. These results suggest that fractalkine and TLR4 may have some inherent relationship, which may play an important role in the development of atherosclerosis.