부산대학교 도서관

To investigate the mechanism of Icariside II (ICSII) in attenuating cardiomyocyte apoptosis in spontaneously hypertensive rats. 96 SPF grade spontaneously hypertensive rats and 24 healthy Wistar rats were randomly selected. The spontaneously hypertensive rats were randomly divided into four groups: model group (n=24), ICSII 10mg/kg dose group (n=24), ICSII 20mg/kg dose group (n=24) and ICSII 30mg/kg dose group (n=24). Healthy Wistar rats served as the control group. Blood pressure, cardiac function indices of rats in each group, histopathological change in the left ventricle of rats in each group and cardiomyocyte apoptosis in rats in each group and the expression of Bcl-2, Bax, Caspase-3, JNK(C-JUN amino terminal kinase), p38, CCAAT/enhancer binding protein homologous protein (CHOP) and glucose regulated protein 78 (GRP78) in the left ventricular tissues of rats in each group were compared. Compared with the control group, LVAWd, LVPWd, LVESD, MDA, JNK, p38, Bax, Caspase-3, GRP78, CHOP levels and left ventricular mass index of rats in the model group were significantly increased, and the cardiomyocyte apoptosis in rats in the model group was significantly increased, but LVFS, LVEF, SOD and Bcl-2 level of rats in the model group were significantly reduced (P<0.05). ICSII can significantly reduce the blood pressure, the level of LVAWd, LVPWd, LVESD, MDA, JNK, p38, Bax, Caspase-3, GRP78, chop level, left ventricular mass index of rats and cardiomyocyte apoptosis in rats, and improve the level of LVFS, LVEF, SOD, bcl-2 of rats, and ICSII 30mg/kg dose group showed the most obvious efficacies. ICSII can significantly attenuate cardiomyocyte apoptosis in spontaneously hypertensive rats by inhibiting oxidative stress, mitochondrial apoptosis signaling pathway and endoplasmic reticulum stress of their myocardial cells. [ABSTRACT FROM AUTHOR]