Lack of Perilipin 5 results in abnormality in mitochondrial functions and aggravates oxidative stress injury of obesity cardiomyopathy

  AIM  To investigate whether Perilipin 5 deficiency may cause abnormal mitochondrial functions in mice, thus exacerbating oxidative stress injury of the myocardium in obesity mice.

  METHODS  For each group of mice, an ultrasound analysis on cardiac function was conducted and the myocardial tissue was observed for myocardial hypertrophy using HE staining method. Malondialdehyde (MDA) and superoxide dismutase (SOD) in myocardial tissue were tested and the secretion levels of mitochondria and Cytochrome C protein in mitochondria and cytoplasm of myocardial tissue were detected using Western blot method.

  RESULTS  Compared with those of ob/ob mice, Compared with ob/ob mice, the heart LVEF and LVIDd of ob/ob/Plin5^-/- mice were further decreased (both P<0.05), LVIDs were further decreased (P<0.01), further increase of cross-sectional area of myocardial cells (P<0.05) and LVPWD (P<0.05), MDA further increased (P<0.01), SOD decreased further (P<0.05). The expression of Cytochrome C protein in myocardial mitochondria was significantly decreased (P<0.01), the expression of Cytochrome C protein in cytoplasm increased significantly (P<0.01).

  CONCLUSION  Plin5 deficiency may aggravate oxidative stress injury of myocardium through interfering with mitochondrial functions, thus causing damage to heart functions in mice.