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

  • Authors:
    • Bo Yang
    • Bin Xu
    • Hua Zhao
    • Ya‑Bin Wang
    • Jian Zhang
    • Chuan‑Wei Li
    • Qing Wu
    • Yu‑Kang Cao
    • Yang Li
    • Feng Cao
  • View Affiliations

  • Published online on: May 16, 2018     https://doi.org/10.3892/mmr.2018.9024
  • Pages: 973-980
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

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 (PARP)/p53 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 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.
View Figures
View References

Related Articles

Journal Cover

July-2018
Volume 18 Issue 1

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Yang B, Xu B, Zhao H, Wang YB, Zhang J, Li CW, Wu Q, Cao YK, Li Y, Cao F, Cao F, et al: Dioscin protects against coronary heart disease by reducing oxidative stress and inflammation via Sirt1/Nrf2 and p38 MAPK pathways. Mol Med Rep 18: 973-980, 2018
APA
Yang, B., Xu, B., Zhao, H., Wang, Y., Zhang, J., Li, C. ... Cao, F. (2018). Dioscin protects against coronary heart disease by reducing oxidative stress and inflammation via Sirt1/Nrf2 and p38 MAPK pathways. Molecular Medicine Reports, 18, 973-980. https://doi.org/10.3892/mmr.2018.9024
MLA
Yang, B., Xu, B., Zhao, H., Wang, Y., Zhang, J., Li, C., Wu, Q., Cao, Y., Li, Y., Cao, F."Dioscin protects against coronary heart disease by reducing oxidative stress and inflammation via Sirt1/Nrf2 and p38 MAPK pathways". Molecular Medicine Reports 18.1 (2018): 973-980.
Chicago
Yang, B., Xu, B., Zhao, H., Wang, Y., Zhang, J., Li, C., Wu, Q., Cao, Y., Li, Y., Cao, F."Dioscin protects against coronary heart disease by reducing oxidative stress and inflammation via Sirt1/Nrf2 and p38 MAPK pathways". Molecular Medicine Reports 18, no. 1 (2018): 973-980. https://doi.org/10.3892/mmr.2018.9024