Dioscin protects against coronary heart disease by reducing oxidative stress and inflammation via Sirt1/Nrf2 and p38 MAPK pathways

作者：Yang, Bo^*; Xu, Bin; Zhao, Hua; Wang, Ya-Bin; Zhang, Jian; Li, Chuan-Wei; Wu, Qing; Cao, Yu-Kang; Li, Yang; Cao, Feng^*

来源：Molecular Medicine Reports, 2018, 18(1): 973-980.

DOI：10.3892/mmr.2018.9024

• dioscin
• coronary heart disease
• inflammation
• sirtuin 1/nuclear factor erythroid 2-related factor 2
• p38 mitogen-activated protein kinase

Cardiovascular diseases arc common diseases in Sweden as in most countries. In 2016, 25,700 persons suffered from coronary heart disease (CHD) and 25% of these died within 28 days. The present study investigated whether dioscin may exert protective effects against CHD-induced heart apoptosis, oxidative stress and inflammation in a pig model and the potential underlying mechanisms. Adult pigs were used to establish a CHD model group and 80 mg/kg dioscin was administered for 4 weeks. Histological analysis and measurement of serum levels of heart injury markers demonstrated that 80 mg/kg dioscin markedly alleviated CHD, while left ventricular ejection fraction and left ventricular systolic internal diameter measurements indicated that 80 mg/kg dioscin also increased heart function in the CHD pig model. Furthermore, western blotting demonstrated that 80 mg/kg dioscin significantly reduced protein levels of apoptosis markers in the heart of CHD model pigs, including Bcl-2-associated X and caspase-3, potentially via the suppression of poly (ADP-ribose) polymerase 1 (PARP)/p53 expression. Additionally, the results of ELBA and western blotting demonstrated that 80 mg/kg dioscin may reduce oxidative stress and inflammation in CHD model pigs through the promotion of sirtuin 1 (Sirt1)/nuclear factor erythroid 2-related factor 2 (Nrf2) protein expression and the suppression of PARP/p53 and p38 mitogen-activated protein kinase (MAPK) expression. The results of the current study indicate that dioscin may protect against CHD by regulating oxidative stress and inflammation via Sirt1/Nrf2 and p38 MAPK pathways.

• 出版日期2018-7
• 单位中国人民解放军总医院