中文摘要：

目的研究甜菜碱对载脂蛋白E（ApoE）基因缺陷小鼠动脉粥样硬化斑块形成的影响并对其抗炎机制进行初步探讨。方法7周龄ApoE基因缺陷小鼠（品系C57BL／6J）按体重随机分为4组：模型组和3个甜菜碱组，同龄同品系野生型小鼠作为正常对照组。各组均喂饲AIN-93G基础饲料，3个甜菜碱组分别加入1％、2％、4％甜菜碱。于0、7、14周时测定血清肿瘤坏死因子-α（TNF-α）、单核细胞趋化蛋白-1、血脂水平以及主动脉TNF—α基因启动子的甲基化状况；于14周时测定主动脉窦脂质斑块占管腔面积百分比。结果2％、4％甜菜碱组主动脉窦斑块面积占管腔总面积百分比分别为（11．43±2．65）％和（12．09±3．07）％，与模型组（19．31±5．42）％相比差异有统计学意义（t值分别为3．117和3．010，P值均小于0．01）；3个甜菜碱组血清TNF-0L分别为（56．33±3．86）、（63．04±4．67）、（65．52±3．97）pg／ml，均明显低于模型组（79．40±4．68）pg／ml（t值分别为9．270、6．571、5．576，P值均小于0．001）。结论甜菜碱可能通过抗炎作用而抑制ApoE基因缺陷小鼠动脉粥样硬化斑块的形成。

英文摘要：

Objective To study the effect of betaine on the formation of atherosclerotic plaque in apolipoprotein E （ApeE）-deficient mice and explore its anti-inflammatory mechanism. Methods Sevenweek-old ApeE-deficient mice （C57BL/6J background） were divided into four groups randomly based on body weight： model group and three betaine groups. Wild-type mice with the same age and genetic background were used as control group. The control group and model group were fed AIN-93G diet. Three betaine groups were fed AIN-93G diet supplemented with 1, 2, 4 g betaine/100 g diet, respectively. Serum tumor necrosis factor-α （TNF-α）, monocyte chemoattractant protein-1, lipid levels and methylation status of TNF-α promotor in arota were determined at 0,7 and 14 weeks. The percentage of arota sinus plaque to lumen area was measured at 14-week. Results The percentage of arota sinus plaque to lumen area of 1% and 2% betaine groups were （ 11.43 ± 2. 65 ） % and （ 12. 09± 3.07） %, respectively, which were 41% and 33% smaller than that of the model group （ t = 3. 117,3. 010, respectively, and P 〈 0. 01 ）. Serum TNF-α level of three betaine groups were （ 56. 33 ± 3.86 ）, （ 63.04 ± 4. 67 ） and （ 65.52 ± 3.97 ） pg/ml, respectively, which were lower than that of the model group （79.40 ±4. 68） pg/ml （t =9. 270,6. 571 and 5. 576,respectively, P 〈 0. 001 ）, but there was no significant difference in the methylation status of TNF-α promotor among all five groups. Conclusion Betaine could inhibit the development of atheroselerosis via anti-inflammation.