中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2009年
1期
59-62
,共4页
沈粤春%陆东风%吴峻%潘洁贞%赵超尘%胡德喜%李君
瀋粵春%陸東風%吳峻%潘潔貞%趙超塵%鬍德喜%李君
침월춘%륙동풍%오준%반길정%조초진%호덕희%리군
动脉粥样硬化%纤维蛋白%遗传
動脈粥樣硬化%纖維蛋白%遺傳
동맥죽양경화%섬유단백%유전
Atheroscleroeis: Fibrin%Heredity
目的 评价凝血因子V莱顿突变(FvL)对动脉粥样硬化的影响.方法 建立FvL与载脂蛋白E(ApoE)基因复合突变小鼠,并分析其动脉粥样硬化形成和纤维蛋白沉积情况.结果 小鼠52周龄时,FvL纯合子ApoE-/-(FvQ/Q APOE-/-)小鼠动脉粥样硬化范围明显大于野生型ApoE-/-(Fv+/+ApoE-/-),小鼠,FvQ/Q ApoE-/-比Fv+/+ApoE-/-为(5.0±1.1)%比(2.2±0.4)%,P＜0.005;FvL杂合子ApoE-/-(FvQ/+ApoE-/-)小鼠动脉粥样硬化范围位于FvQ/Q ApoE-/-小鼠和Fv+/+ApoE-/-小鼠之间,与两者的差异均无统计学意义,FvQ/+ApoE-/-比FvQ/QApoE-/-为(2.9±0.6)%比(5.0.±1.1)%,P＞0.05,FvQ/+ApoE-/-比Fv+/+ApoE-/-为(2.9±0.6)%比(2.2±0.4)%,P＞0.05.FvQ/Q ApoE-/-小鼠动脉粥样硬化斑块内的纤维蛋白沉积同样明显高于Fv+/+ApoE-/-小鼠,FvQ/Q ApoE-/-比Fv+/+ApoE-/-为(3.4±0.5)%比(1.8±0.4)%,P＜0.05.结论 FvL纯合子明显增加ApoE-/-小鼠动脉粥样硬化程度及动脉粥样硬化斑块内的纤维蛋白沉积,提示FvL突变可能是重要的促进动脉粥样硬化形成的因素,临床上患者出现严重的动脉粥样硬化可能合并FvL遗传基因缺陷.
目的 評價凝血因子V萊頓突變(FvL)對動脈粥樣硬化的影響.方法 建立FvL與載脂蛋白E(ApoE)基因複閤突變小鼠,併分析其動脈粥樣硬化形成和纖維蛋白沉積情況.結果 小鼠52週齡時,FvL純閤子ApoE-/-(FvQ/Q APOE-/-)小鼠動脈粥樣硬化範圍明顯大于野生型ApoE-/-(Fv+/+ApoE-/-),小鼠,FvQ/Q ApoE-/-比Fv+/+ApoE-/-為(5.0±1.1)%比(2.2±0.4)%,P＜0.005;FvL雜閤子ApoE-/-(FvQ/+ApoE-/-)小鼠動脈粥樣硬化範圍位于FvQ/Q ApoE-/-小鼠和Fv+/+ApoE-/-小鼠之間,與兩者的差異均無統計學意義,FvQ/+ApoE-/-比FvQ/QApoE-/-為(2.9±0.6)%比(5.0.±1.1)%,P＞0.05,FvQ/+ApoE-/-比Fv+/+ApoE-/-為(2.9±0.6)%比(2.2±0.4)%,P＞0.05.FvQ/Q ApoE-/-小鼠動脈粥樣硬化斑塊內的纖維蛋白沉積同樣明顯高于Fv+/+ApoE-/-小鼠,FvQ/Q ApoE-/-比Fv+/+ApoE-/-為(3.4±0.5)%比(1.8±0.4)%,P＜0.05.結論 FvL純閤子明顯增加ApoE-/-小鼠動脈粥樣硬化程度及動脈粥樣硬化斑塊內的纖維蛋白沉積,提示FvL突變可能是重要的促進動脈粥樣硬化形成的因素,臨床上患者齣現嚴重的動脈粥樣硬化可能閤併FvL遺傳基因缺陷.
목적 평개응혈인자V래돈돌변(FvL)대동맥죽양경화적영향.방법 건립FvL여재지단백E(ApoE)기인복합돌변소서,병분석기동맥죽양경화형성화섬유단백침적정황.결과 소서52주령시,FvL순합자ApoE-/-(FvQ/Q APOE-/-)소서동맥죽양경화범위명현대우야생형ApoE-/-(Fv+/+ApoE-/-),소서,FvQ/Q ApoE-/-비Fv+/+ApoE-/-위(5.0±1.1)%비(2.2±0.4)%,P＜0.005;FvL잡합자ApoE-/-(FvQ/+ApoE-/-)소서동맥죽양경화범위위우FvQ/Q ApoE-/-소서화Fv+/+ApoE-/-소서지간,여량자적차이균무통계학의의,FvQ/+ApoE-/-비FvQ/QApoE-/-위(2.9±0.6)%비(5.0.±1.1)%,P＞0.05,FvQ/+ApoE-/-비Fv+/+ApoE-/-위(2.9±0.6)%비(2.2±0.4)%,P＞0.05.FvQ/Q ApoE-/-소서동맥죽양경화반괴내적섬유단백침적동양명현고우Fv+/+ApoE-/-소서,FvQ/Q ApoE-/-비Fv+/+ApoE-/-위(3.4±0.5)%비(1.8±0.4)%,P＜0.05.결론 FvL순합자명현증가ApoE-/-소서동맥죽양경화정도급동맥죽양경화반괴내적섬유단백침적,제시FvL돌변가능시중요적촉진동맥죽양경화형성적인소,림상상환자출현엄중적동맥죽양경화가능합병FvL유전기인결함.
Objective Factor V Leiden(FvL)causing activated protein C resistance is a genetic risk factor for venous thrombosis in humans,and it's effect on atherosclemsis is controversial.We evaluated the effect of FvL mutation on atherosclerosis in apolipoprotein E deftcient mice fed with normal diet.Methods Degree of atherosclerosis and tissue fibrin deposition were determined in Fv+/+ApoE-/-,FvQ/ApoE-/-and FvQ/QApoE-/-mice.Results In the presence of ApoE deficiency.homozygous FvL significandy increased atherosclerosis coverage in ApoE-/-mice(FvQ/QApoE-/-vs.Fv+/+ApoE-/-=5.0%±1.1%vs.2.2%±0.4%,P＜0.005)and tissue fibrin deposition in atherosclerotic lesion(FvQ/QApoE-/-vs.Fv+/ApoE-/-=3.4%±0.5%vs.1.8%±0.4%,P＜0.05).The atherosclerotic Iesion of FvQ/+ApoE-/-mice was intermediate between FvQ/Q ApoE -/-and Fv+/ApoE-/-,and there was no significant difference comparing with any of them.Condusions Therie observations demonstrate that homozygous FvL could promote atherosclerosis and fibrin deposition in apolipoprotein E deficient mice suggesting that Factor V mutation could be an important genetic risk factor for the enhanced atherosclerosis in human.
