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目的观察高脂血症大鼠心肌与肾皮质微细结构的改变,探讨人体重要脏器微血管及实质细胞损伤与冠心病形成、发展的关系。方法 20只雄性SD大鼠,随机分成对照组与实验组,每组10只。实验组以高脂饮食制作高脂血症病理模型,对照组普通动物饲料喂食。喂养8周后,处死大鼠,右心房采血,分别采用用总胆固醇酶法(COD-PAP)、甘油三酯酶法(GPO-PAP)和过氧化氢酶(CAT)法检测血清胆固醇(TCH)、甘油三酯(TG)及高密度脂蛋白胆固醇(HDL-C)与低密度脂蛋白胆固醇(LDL-C);制作心脏与肾脏切片,采用HE染色和免疫组化PV-9000二步法染色,光镜观察心肌与肾皮质的微细结构及作为凋亡相关因子的死亡因子(Fas-L)与细胞骨架相关的肌动蛋白(Actin)的表达,Mimics10.0行图像灰度分析,SPSS13.0行统计学分析。结果实验组大鼠血清TCH、TG及HDL-C、LDL-C水平均高于对照组(P<0.05,P<0.01),显示大鼠高脂血症模型制备成功。实验组心肌与肾皮质间质增宽,微静脉与毛细血管扩张并淤血,小动脉与微动脉内皮细胞增多,内膜增厚,局部隆起,管腔内可见微血栓。心肌内有小片状变性、坏死区与散在变性、坏死的肌纤维,肾皮质血管球扩张与淤血,肾小管上皮细胞变性与坏死,管腔内有空泡与絮状物。图像灰度分析显示,实验组Actin表达的灰度值明显高于对照组(P<0.05),Fas-L心肌、肾皮质的表达明显低于对照组(P均<0.05)。结论高脂血症可能通过增加Fas-L在心肌、肾皮质的表达,减少Actin在心肌的表达引起大鼠心肌与肾皮质微血管和实质细胞结构发生改变,推测可能与冠心病形成与发展有着密切的关系。
Objective To observe the changes of myocardial and renal cortical ultrastructure in hyperlipidemic rats, and to explore the relationship between microvascular and parenchymal cell damage in important organs of human and the formation and development of coronary heart disease. Methods Twenty male SD rats were randomly divided into control group and experimental group with 10 rats in each group. Experimental group with hyperlipidemia hyperlipemia pathological model, the control group fed ordinary animal feed. After feeding for 8 weeks, the rats were sacrificed and the right atrium was collected for blood sampling. Serum cholesterol (TCH) was measured by total cholesterol (COD-PAP), triglyceride (GPO-PAP) and catalase (CAT) TG, HDL-C and LDL-C. Cardiac and kidney sections were made by HE staining and immunohistochemistry PV-9000 two-step method Staining, light microscopy myocardial and renal cortex microstructure and death-related factors (Fas-L) and cytoskeletal-related actin (Actin) expression, Mimics10.0 line grayscale analysis, SPSS13 .0 line statistical analysis. Results The levels of serum TCH, TG, HDL-C and LDL-C in the experimental group were significantly higher than those in the control group (P <0.05, P <0.01), indicating that the model of hyperlipidemia was successfully established in the experimental group. Experimental group myocardial and renal cortex interstitial broadening, venules and telangiectasia and congestion, arteriolar and arteriolar endothelial cells increased, thickening of the intima, local uplift, visible micro-thrombosis within the lumen. Small pieces of degeneration in the myocardium, necrosis of the area and scattered degeneration, necrosis of the muscle fibers, renal cortical dilatation and congestion of the blood vessels, renal tubular epithelial cell degeneration and necrosis, the cavity with vacuoles and floccules. The grayscale analysis showed that the gray value of Actin in the experimental group was significantly higher than that in the control group (P <0.05), and the expression of Fas-L in myocardium and renal cortex was significantly lower than that in the control group (all P <0.05). Conclusion Hyperlipidemia may change the structure of microvascular and parenchymal cells in myocardium and renal cortex of rats by increasing the expression of Fas-L in myocardium and renal cortex and decreasing the expression of Actin in myocardium, which may be closely related to the formation and development of coronary heart disease Relationship.