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作 者:徐戈[1] 黄琛 李志乐[3] 文伟明[1] 欧婷[1] 王利兵[1]
机构地区:[1]广西医科大学第一附属医院心内科,南宁530021 [2]西中医药大学第一附属医院干部保健科 [3]广西右江民族医学院附属医院心内科
出 处:《中华老年心脑血管病杂志》2013年第10期1072-1076,共5页Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基 金:广西科学基金项目(0832049)
摘 要:目的探讨烟酸对高脂血症免动脉粥样硬化斑块和TC逆转运相关基因表达的影响。方法24只兔分为对照组、高脂组和烟酸组,每组8只。实验前后检测血脂水平;14周末行主动脉病理学检测;采用实时荧光定量PCR检测ATP结合盒转运体A1(ABCA1)、B族I型清道夫受体(SR-BI)和小凹蛋白1(Cav-1)mRNA表达。体外观察不同浓度烟酸(0-5.0mmol/L)对Filipin阻断后ABCA1、SR-BI和Car-1表达的影响。结果与对照组比较,高脂组8周时TC、TG和LDL-c、主动脉内膜厚度和斑块面积明显增加,ABCA1、sR-BI和Cav-1mRNA表达明显降低(P〈0.05,P〈0.01)。与高脂组比较,烟酸组14周时TC、TG和I.DL-C明显降低,HDL-C、ABCA1和Cav-1mRNA表达明显升高,主动脉内膜厚度和斑块面积明显缩小(P〈0.01)。1.0mmol/L烟酸可明显改善Cav-1与ABCA1mRNA表达(P〈0.05)。结论烟酸可明显改善血脂谱及稳定动脉粥样硬化斑块,上调ABCA1与Car-1mRNA表达水平,但对SR-BI表达无明显影响。Objective To study the effect of niacin on atherosclerotic plaques and reverse cholester- ol transport-related gene expression in hyperlipidemia rabbits. Methods Twenty-four rabbits were randomly divided into control group, hyperlipidemia group and niacin group (8 in each group). Their blood lipid level was measured before and after experiment. The animals underwent pathological examination by the end of 14 weeks. Expressions of ABCA1,SR-B I and Cav-1 mRNA in primary rabbit adipocytes were detected by RT-PCR. Effect of niacin at different concentrations (0-5.0 retool/L) on filipin-blocked expressions of ABCA1,SR-B I and Cav-1 mRNA was ob- served. Results The serum TC,TG and I.DL-C levels,aortic IMT and plaque area were signifi- cantly higher while the expression levels of ABCAI ,SR-B I and Cav-1 mRNA were significantly lower in hyperlipidemia group than in control group (P〈0.05, P〈0.01). The serum TC, TG and I.DL-C levels were significantly lower, the serum HDL-C level was significantly higher, and the aortic IMT and plaque area were significantly smaller in niacin group than in hyperlipidemia group (P〈0. 01). Niacin (1. 0 retool/L) could effectively improve the filipin-bloeked expressions of ABCA1,SR-B i and Cav-1 mRNA (P〈0.05). Conclusion Niacin can significantly improve the lipid profile and stabilize the atherosclerotic plaques, upregulate the expression of ABCA1 and Cav-1 mRNA,and regulate the expression of ABCA1 mRNA via the Cav-1 gene.
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