中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2010年
9期
809-813
,共5页
黄贤圣%赵水平%柏林%张骞%胡敏%赵旺
黃賢聖%趙水平%柏林%張鶱%鬍敏%趙旺
황현골%조수평%백림%장건%호민%조왕
载脂蛋白A类%甘油三酯类%PPARα%他汀类药物
載脂蛋白A類%甘油三酯類%PPARα%他汀類藥物
재지단백A류%감유삼지류%PPARα%타정류약물
Apolipoproteins A%Triglycerides%PPAR alpha%Statins
目的 明确他汀降低甘油三酯(TG)作用是否与载脂蛋白A5(ApoA5)有关,探讨他汀调节ApoA5的机制.方法 24只Sprague-Dawley大鼠随机分为3组:(1)对照组(n=8):正常普通饮食喂养;(2)高甘油三酯血症(HTG)组(n=8):10%果糖水喂养2周建立HTG大鼠模型,并继续喂养4周;(3)他汀组(n=8):HTG大鼠建模后,加予阿托伐他汀(10 mg·kg-1·d-1)干预4周.测定空腹血脂及肝脏ApoA5和过氧化物酶体增殖物激活受体α(PPARα)表达.体外观察阿托伐他汀对HepG2细胞TG、ApoA5和PPARα的影响,并检测PPARα抑制剂是否影响他汀的上述效应.结果 (1)6周后,HTG组大鼠TG显著高于对照组,而他汀组TG则显著低于HTG组(P均<0.05).(2)HTG组大鼠ApoA5表达显著低于对照组,而他汀组的ApoA5表达则显著高于HTG组(P均<0.05).(3)HTG组大鼠PPARα的mRNA表达显著低于对照组,而他汀组PPARα mRNA表达显著高于HTG组(P均<0.05).结论 他汀显著升高肝细胞ApoA5和PPARα表达,降低细胞TG含量,但PPARα抑制剂可以显著抑制他汀的上述效应.他汀通过PPARα通路,上调ApoA5表达,降低TG.
目的 明確他汀降低甘油三酯(TG)作用是否與載脂蛋白A5(ApoA5)有關,探討他汀調節ApoA5的機製.方法 24隻Sprague-Dawley大鼠隨機分為3組:(1)對照組(n=8):正常普通飲食餵養;(2)高甘油三酯血癥(HTG)組(n=8):10%果糖水餵養2週建立HTG大鼠模型,併繼續餵養4週;(3)他汀組(n=8):HTG大鼠建模後,加予阿託伐他汀(10 mg·kg-1·d-1)榦預4週.測定空腹血脂及肝髒ApoA5和過氧化物酶體增殖物激活受體α(PPARα)錶達.體外觀察阿託伐他汀對HepG2細胞TG、ApoA5和PPARα的影響,併檢測PPARα抑製劑是否影響他汀的上述效應.結果 (1)6週後,HTG組大鼠TG顯著高于對照組,而他汀組TG則顯著低于HTG組(P均<0.05).(2)HTG組大鼠ApoA5錶達顯著低于對照組,而他汀組的ApoA5錶達則顯著高于HTG組(P均<0.05).(3)HTG組大鼠PPARα的mRNA錶達顯著低于對照組,而他汀組PPARα mRNA錶達顯著高于HTG組(P均<0.05).結論 他汀顯著升高肝細胞ApoA5和PPARα錶達,降低細胞TG含量,但PPARα抑製劑可以顯著抑製他汀的上述效應.他汀通過PPARα通路,上調ApoA5錶達,降低TG.
목적 명학타정강저감유삼지(TG)작용시부여재지단백A5(ApoA5)유관,탐토타정조절ApoA5적궤제.방법 24지Sprague-Dawley대서수궤분위3조:(1)대조조(n=8):정상보통음식위양;(2)고감유삼지혈증(HTG)조(n=8):10%과당수위양2주건립HTG대서모형,병계속위양4주;(3)타정조(n=8):HTG대서건모후,가여아탁벌타정(10 mg·kg-1·d-1)간예4주.측정공복혈지급간장ApoA5화과양화물매체증식물격활수체α(PPARα)표체.체외관찰아탁벌타정대HepG2세포TG、ApoA5화PPARα적영향,병검측PPARα억제제시부영향타정적상술효응.결과 (1)6주후,HTG조대서TG현저고우대조조,이타정조TG칙현저저우HTG조(P균<0.05).(2)HTG조대서ApoA5표체현저저우대조조,이타정조적ApoA5표체칙현저고우HTG조(P균<0.05).(3)HTG조대서PPARα적mRNA표체현저저우대조조,이타정조PPARα mRNA표체현저고우HTG조(P균<0.05).결론 타정현저승고간세포ApoA5화PPARα표체,강저세포TG함량,단PPARα억제제가이현저억제타정적상술효응.타정통과PPARα통로,상조ApoA5표체,강저TG.
Objective To explore the potential role of apolipoprotein A5 (apoA5) on the hypertriglyceridemia (HTG)-lowering effects of statin. Methods Twenty-four Sprague-Dawley rats were randomized into 3 groups: ( 1 ) control group ( n = 8), with no special treatment; (2) HTG group (n = 8),treated with 10% fructose water for 6 weeks; (3) statin group(n =8), treated with 10% fructose water for lipids and the hepatic expressions of apoA5 and peroxisome proliferstor activated receptor (PPAR)α were determined. In separate in vitro experiments, we tested the effects of atorvastatin on TG and the expressions of apoA5 and PPARα in HepG2 cells. Results ( 1 ) At 6 weeks, plasma TG was higher in rats in HTG group than in controls, which was significantly reduced in statin group (both P <0. 05). (2) Rat hepatic apoA5 expression in HTG group was significantly lower than in control group and was significantly higher in statin group than in HTG group ( both P < 0. 05 ). (3) Similarly, rat PPARα mRNA expression in HTG group was lower than in control group and was higher in statin group than in HTG group ( both P < 0. 05 ).(4) Statin significantly upregulated the expressions of apoA5 and PPARα and decreased TG in HepG2 cells.The above effects induced by statin was blocked in the presence of PPARα inhibitor. Conclusions Upregulation of apoA5 expression contributes to TG lowering effect of statin via PPARα signaling pathway.
