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

Cardiovascular diseases are 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 expression. Additionally, the results of ELISA 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 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.

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