阿托伐他汀对兔主动脉粥样硬化斑块和脂肪酸结合蛋白的抑制作用

目的观察阿托伐他汀对兔动脉粥样硬化斑块和血清脂肪细胞型脂肪酸结合蛋白(AFABP)的作用机制。方法 16只新西兰大白兔给予高TC饲料饲养8周后,随机分为高TC组(继续饲以高TC饲料4周)和阿托伐他汀组(在饲以高TC饲料的基础上给予阿托伐他汀2.5 mg·kg~(-1)·d~(-1)4周),每组8只。另选8只普通饲料饲养12周的新西兰大白兔作为对照组。分析观察前、8和12周兔血脂和AFABP水平的变化;12周末处死兔,取主动脉进行病理学检查;RT-PCR测定主动脉AFABP mRNA的表达。结果与高TC组比较,阿托伐他汀组兔12周时血清TC、LDL-C、AFABP水平和AFABP mRNA表达均明显降低(P0.01)。对照组、高TC组、阿托伐他汀组斑块/内膜面积比分别为0、(75.80±8.21)%和(46.11±3.56)%,差异显著(P0.01);内膜厚度分别为(4.12±0.29)μm、(74.18±10.25)μm和(39.45±5.68)μm;内膜/中膜比分别为0.05±0.01、0.85±0.31和0.48±0.23,差异显著(P0.01)。结论阿托伐他汀具有抗动脉粥样硬化作用,其降低兔血清AFABP水平及主动脉AFABP mRNA的表达可能是其作用机制之一。

Inhibitory effect of atorvastatin on aortic atherosclerotic plaque and levels of serum adipocyte fatty acid-binding protein in rabbits

Objective To examine the mechanism of effects of atorvastatin on aortic atherosclerotic plaque and serum adipocyte fatty acid-binding protein(AFABP) in rabbits.Methods Sixteen New Zealand white rabbits were fed with high cholesterol diet for 8 weeks,and were randomly divided into two groups:high cholesterol group(maintaining cholesterol diet for 4 weeks) and atorvastatin group(fed with same cholesterol diet supplemented with atorvastatin 2.5 mg·kg~(-1)·d~(-1) for 4 weeks).Other 8 rabbits served as control group and were fed with normal diet for 12 weeks.Be fore and after feeding,serum lipid and AFABP levels in rabbits were measured.After 12 weeks, the aorta was harvested for pathomorphological observation,AFABP mRNA expression in aorta was evaluated by RT-PCR.Results TC,LDL-C,AFABP and AFABP mRNA expression in atorvastatin group were greatly lower than those in high cholesterol group.The aorta plaque/intima size was 0,(75.80±8.21) % and (46.11±3.56) % in the three groups respectively (P < 0.01); intima thickness was(4.12±0.29) μm,(74.18±10.25) μm and (39.45 ± 5.68) μm respectively; intima/media thickness ratio(I/M) was 0.05 ± 0.01,0.85 ± 0.31 and 0.48 ± 0.23 respectively (P < 0.01).Conclusions The results indicate that atorvastatin has anti-atheromatous effect,decreases serum AFABP levels and the inhibition of AFABP mRNA expression in aorta may be one of anti-atheromatous mechanisms.