摘要
目的建立食源性高脂血症大鼠心肌缺血/再灌注模型,观察吡格列酮对高脂血症并发缺血/再灌注大鼠心肌细胞膜流动性的影响。方法 Wistar大鼠随机分为对照组(基础饲料喂养)、高脂组(高脂饲料喂养)。4周后,高脂组大鼠再随机分为高脂组和高脂+吡格列酮干预组,8周末实施心肌缺血/再灌注,通过Langendorff灌流装置酶液灌流分离单个心肌细胞,利用荧光标记物DPH插入其细胞膜脂质双层,测定荧光偏振值(ρ),并计算膜脂微黏度(η)。4周和8周(实验期末)末分别采血,检测血清中总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDLC)含量。实验期末测定谷胱甘肽过氧化物酶(GPX)、超氧化物歧化酶(SOD)和丙二醛(MDA)的含量。结果与对照组比较,高脂组血清中TG、TC、HDLC含量显著升高(P<0.05);吡格列酮组与高脂组比较可显著降低血清中TG、TC含量(P<0.01);吡格列酮使血清中MDA含量下降(P<0.05),GPX和SOD活性上升(P<0.05);吡格列酮组荧光偏振度ρ值和膜脂微黏度η值均小于高脂组(P<0.05)。结论吡格列酮保护心肌细胞膜的正常流动性,可能与其降脂、抗氧化保护细胞膜的结构相关。
Aim Using hyperlipemia rats induced by diets with myocardial ischemia/reperfusion, to observe the effects of pioglitazone （PI） on myocardial cell membrane fluidity. Methods Wistar rats were randomized into 2 groups： control group （C） was fed with normal diets and the hyperlipemia group （HL） was fed with high cholesterol diets. After 4 weeks, The HL group was divided into HL and HL ＋ PI groups. At the end of the 8 weeks, ischemic/reperfusion in vivo was carried out and single myocardial cell was separated by the enzyme perfusion with the apparatus of Langendorff. The cardiomyocyte membrane fluidity was determined by DPH marking method and the value of fluorescence polarization （p） and the microviscosity of membrane lipid （η） was calculated. The levels of serum triglycerides （TG）, total choles- terol （TC） and high density lipoprotein cholesterol （HDLC） were tested by kits at the end of 4 weeks and 8 weeks. The content of malondialdehyde （MDA） in the serum, the activities of superoxide dismutase （SOD） and glutathione peroxidase （GPX） were respectively determined. Results The levels of serum TG, TC and HDLC in the high cholesterol diets rats increased subjected to normal diets rats （P〈0.05） ;Treatment with pioglitazone in HL rats decreased the levels of ser- um TG and TC, compared with HL group （P〈0.01） ;HL ＋ PI decreased the levels of MDA and increased the activities of SOD and GPX （P〈0.05） ;（4）The p and η in HL ＋ PI group were less than HL group （P〈0.05）.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2013年第5期409-413,共5页
Chinese Journal of Arteriosclerosis
基金
山西省高校科技研究开发项目(200611016)
