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作 者:钟建开[1] 郭志刚[1] 李琛[1] 王振坤[1] 赖文岩[1] 刘爱华[1]
机构地区:[1]南方医科大学南方医院心内科,广州510515
出 处:《中华老年心脑血管病杂志》2010年第11期1024-1027,共4页Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基 金:广东省科技计划(2008B030301158);南方医科大学南方医院院长重点基金(2008A003)
摘 要:目的研究普罗布考对动脉粥样硬化(AS)兔HDL亚组分及氧化功能的影响,探讨普罗布考抗AS机制。方法选择18只新西兰大白兔随机分为:对照组6只,饲以普通饲料;AS组6只,饲以高脂饲料;普罗布考组6只,饲以高脂饲料基础上给予普罗布考400 mg/(kg·d)。1 2周后酶法检测血脂;分光光度计法检测血清对氧磷酶1(PON1)活性;采用化学沉淀法检测HDL_2/HDL;组织切片和HE染色检测主动脉内膜中层厚度(IMT)和动脉斑块/血管面积。结果实验12周后,与AS组比较,普罗布考组血清TC、LDL-C、HDL-C水平明显下降(P<0.01);PON1活性明显升高(P=0.000);HDL_2/HDL明显降低(P=0.000),主动脉IMT明显减小(P=0.000),斑块面积/血管腔面积明显降低(P=0.002)。结论普罗布考通过提高PON1活性,降低HDL_2/HDL而改善HDL功能,减少主动脉IMT及斑块面积/血管腔面积,延缓AS进展。Objectives To investigate the effect of probucol on HDL subfractions and anti-oxidation function and explore the anti-atherosclerosis mechanisms of probucol. Methods Eighteen rabbits were randomly divided into three groups: control group (n = 6): fed with normal diet for 12 weeks;atherosclerosis(AS) group (n = 6):fed with high-fat diet for 12 weeks;probucol group (n =6):fed with high-fat diet plus probucol 400 mg/(kg · d) for 12 weeks. Serum lipids levels were determined by enzymatic methods, HDL2/HDL ratio was determined by chemical precipitation method and the plasma paraoxonase 1(PON1) activity was assessed by spectrophotometry using phenylacetate as substrate. The aorta was excised for investigating the histological characteristics at the end of 12 weeks after confirmation of death of the rabbits. Results Compared with AS group,the levels of serum total cholesterol, low-density lipoprotein cholesterol, high density lipoprotein cholesterol (P 〈 0. 01) and HDL2/HDL ratio (P = 0. 000) were significantly reduced,while plasma PON1 activity significantly euhanced (P = 0. 000) in probucol group. The aortic intima-media thickness (P = 0. 000) and the percentage of plaque area (P = 0. 002) were significantly smaller in probucol group compared with AS group. Conclusions Probucol can reduce the formation of aortic plaques and has effect of improving HDL function through increasing plasma PON1 activity and changing the ratio of HDL subfraction, thus delaying the progress of AS.
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