Abstract

Background: In recent years, relevant studies had shown that a large number of adipokines were involved in energy homeostasis in the body, regulating the balance of glucose and lipid metabolism. Resistin was a special type of adipose factor and its discovery and related studies had shown a close relationship between resistin and heart disease. However, there was relatively little research on the structure of heart tissue, so we conducted this present study. Methods: In order to study the effect of resistin on the heart structure of mice, 20 healthy C57BL/6 mice were randomly divided into experimental and control groups(n=10). The mice of the experimental group were injected with 20 ìl/d of resistin solution through the tail vein. The mice of the control group were injected with the same volume of double distilled water. HandE staining, Wheat Germ Agglutinin (WGA) staining, Masson’s trichrome staining and electron microscopy were used to observe the changes of microscopic structure and ultrastructure of mouse cardiomyocytes. Result: The results of HandE staining showed that the myocardial cells in the experimental group were disordered, the cytoplasm was loosely distributed and the gap between adjacent cells increased. WGA staining showed that the fluorescence green intensity of the mice in the experimental group was higherthan that of the control group. The myocardial cell membrane thickened, the average cross-sectional area of cardiomyocytes was larger than that of the control group. The results of the Masson staining showed that the staining of the cytoplasm of myocardial cells in the experimental group was significantly shallow and the blue structure was significantly increased. The electron microscopy showed that the number of mitochondria decreased and the mitochondria lightly dissolved or disappear. This study confirmed that resistin could change the content of collagen fibers and myofibrils in myocardial cells, induce cardiac hypertrophy and cause certain damage to mitochondria of cardiomyocytes. It was speculated that it could affect the physiological function of cardiomyocytes to some extent.

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