烟酸对幼年肥胖大鼠血脂及血管内皮粘附功能的影响

目的研究烟酸对幼年肥胖大鼠血脂及血管内皮粘附功能的影响,探讨烟酸防治动脉粥样硬化(AS)的作用机制。方法Wistar大鼠随机分为对照组和试验组,分别饲予基础饲料和高脂饲料,8周后肥胖大鼠造模成功。肥胖大鼠再随机分为3组:A组:单纯控制食谱,B组:控制食谱+烟酸,F组:继续高脂饮食。原对照组继续饲予基础饲料,为N组。干预12周后,处死全部大鼠,测定血脂指标:总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)、计算动脉粥样硬化指数(AI);血管内皮粘附因子:血清可溶性细胞间粘附分子1(sICAM-1),免疫组化法检测腹主动脉ICAM-1蛋白的表达,RT-PCR法检测腹主动脉ICAM-1mRNA的表达。结果与F组比较,B组的TC、TG、LDL、AI、sICAM-1、ICAM-1蛋白和mRNA表达水平显著降低,HDL显著升高,且均与N组无显著差异。结论控制食谱联合烟酸可以改善血脂、血管内皮粘附功能,因此调节血脂紊乱和血管内皮粘附功能障碍是烟酸类药物改善AS预后的可能机制。

The study of niacin's effect on serum lipid and vasular endothelial adhesion dysfunction of Juvenile obese rats

Objective To observe the effect of diet-control with niacin on the serum lipid level and vascular endothelial adhesion in juvenile obese rats fed by fat-rich-diet. Methods Thirty-two Wistar rats were randomly divided into control group(n=8), which were given basic-diet and experimental group(n=24), which were given fat-rich-diet. After 8 weeks, the animal model of obesity had been made successfully. Then the fat rats were randomly divided into 3 subgroups: subgroup A: received diet-control only; subgroup B: received diet-control with niacin; subgroup F: received fat-rich-diet continuously. The control group(group N)was given basic-diet continuously. All rats were killed after 12 weeks of intervention. Then the levels of serum total cholesterol(TC), triglyceride(TG), high density lipoprotein(HDL), low density lipoprotein(LDL), atherosclerotic index(AI), soluble intercellular adhesion molecule-1(sICAM-1)were detected. The protein expression of ICAM-1 in artery endothelium was evaluated by immunohistochemistry(IHC)and the gene expression of ICAM-1 was examined by semi-quantitative RT-PCR. Results Comparing with group F, the levels of TC, TG, LDL, AI, sICAM-1, the protein and gene expression of ICAM-1 in artery endothelium decreased in group B, the levels of HDL increased in group B. The levels of index above in group B were equal with group N. Conclusion Diet-control with niacin can meliorate the hyperlipidemia and vascular adhesion dysfunction.