中华预防医学杂志
中華預防醫學雜誌
중화예방의학잡지
CHINESE JOURNAL OF
2008年
10期
742-747
,共6页
范锐心%吕史维%杜艳平%侯孟君%朱惠莲
範銳心%呂史維%杜豔平%侯孟君%硃惠蓮
범예심%려사유%두염평%후맹군%주혜련
甜菜碱%动脉硬化%小鼠,基因敲除%炎症%甲基化
甜菜堿%動脈硬化%小鼠,基因敲除%炎癥%甲基化
첨채감%동맥경화%소서,기인고제%염증%갑기화
Betalne%Arteriosclerosis%Mice,knockout%Inflammation%Methylation
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)%,与模犁组(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-α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 甜菜碱口J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.
目的 研究甜菜堿對載脂蛋白E(ApoE)基因缺陷小鼠動脈粥樣硬化斑塊形成的影響併對其抗炎機製進行初步探討.方法 7週齡ApoE基因缺陷小鼠(品繫C57BL/6J)按體重隨機分為4組:模型組和3箇甜菜堿組,同齡同品繫野生型小鼠作為正常對照組.各組均餵飼AIN-93G基礎飼料.3箇甜菜堿組分彆加入1%、2%、4%甜菜堿.于0、7、14週時測定血清腫瘤壞死因子-α(TNF-α)、單覈細胞趨化蛋白-1、血脂水平以及主動脈TNF-α基因啟動子的甲基化狀況;于14週時測定主動脈竇脂質斑塊佔管腔麵積百分比.結果 2%、4%甜菜堿組主動脈竇斑塊麵積佔管腔總麵積百分比分彆為(11.43±2.65)%和(12.09 ±3.07)%,與模犛組(19.31±5.42)%相比差異有統計學意義(t值分彆為3.117和3.010,P值均小于0.01);3箇甜菜堿組血清TNF-α分彆為(56.33±3.86)、(63.04±4.67)、(65.52±3.97)pg/ml,均明顯低于模型組(79.40 ±4.68)pg/ml(t值分彆為9.270、6.571、5.576,P值均小于0.001).結論 甜菜堿口J能通過抗炎作用而抑製ApoE基因缺陷小鼠動脈粥樣硬化斑塊的形成.
목적 연구첨채감대재지단백E(ApoE)기인결함소서동맥죽양경화반괴형성적영향병대기항염궤제진행초보탐토.방법 7주령ApoE기인결함소서(품계C57BL/6J)안체중수궤분위4조:모형조화3개첨채감조,동령동품계야생형소서작위정상대조조.각조균위사AIN-93G기출사료.3개첨채감조분별가입1%、2%、4%첨채감.우0、7、14주시측정혈청종류배사인자-α(TNF-α)、단핵세포추화단백-1、혈지수평이급주동맥TNF-α기인계동자적갑기화상황;우14주시측정주동맥두지질반괴점관강면적백분비.결과 2%、4%첨채감조주동맥두반괴면적점관강총면적백분비분별위(11.43±2.65)%화(12.09 ±3.07)%,여모리조(19.31±5.42)%상비차이유통계학의의(t치분별위3.117화3.010,P치균소우0.01);3개첨채감조혈청TNF-α분별위(56.33±3.86)、(63.04±4.67)、(65.52±3.97)pg/ml,균명현저우모형조(79.40 ±4.68)pg/ml(t치분별위9.270、6.571、5.576,P치균소우0.001).결론 첨채감구J능통과항염작용이억제ApoE기인결함소서동맥죽양경화반괴적형성.
Objective To study the effect of betaine on the formation of atherosclerotic plaque in apolipoprotein E ( ApoE ) -deficient mice and explore its anti-inflammatory mechanism. Methods Seven-week-old ApE-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), monocytc chemoattractant protein-I, 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/nd (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 atherosclerosis via anti-inflammation.
