Wogonoside preserves against ischemia/reperfusion-induced myocardial injury by suppression of apoptosis, inflammation, and fibrosis via modulating Nrf2/HO-1 pathway

Abstract

Objective

Myocardial ischemia/reperfusion (I/R) injury occurs after restoring blood supply, which brings about extra damage to heart tissue. Thus, exploring protection measures and underlying mechanisms appear to be particularly important. In this study, we investigated the cardioprotection of wogonoside against I/R injury in mice and further uncovered its mechanism.

Methods

Mice model of myocardial I/R injury was established by left anterior descending coronary artery (LAD). Before modeling, mice were administered the wogonoside (10, 20, and 40 mg/kg) for 7 d. To evaluate the effect of wogonoside through nuclear factor E2-associated factor 2/heme oxygenase-1 (Nrf2/HO-1) pathway, sh-Nrf2 was transfected into wogonoside-treated I/R mice. Subsequently, echocardiography detection, HE staining, western blotting, ELISA, TUNEL assay, and MASSON assay were utilized to evaluate the degree of myocardial injury.

Results

In I/R group, mice had severe myocardial injury, however, pretreatment of wogonoside at doses of 20 and 40 mg/kg ameliorated the cardiac function, as evidenced by improving hemodynamic parameters. Besides, wogonoside could relieved the abnormality of cardiomyocytes structure, inflammatory reaction, apoptosis, and myocardial fibrosis. Importantly, wogonoside activated the Nrf2/HO-1 pathway, as demonstrated by increasing Nrf2 expression in nucleus and its downstream genes including HO-1 and NADPH quinone oxidoreductase-1 (NQO1). However, effects of wogonoside on cardioprotection were abolished by sh-Nrf2.

Conclusions

Wogonoside exerted the protective role against I/R-induced myocardial injury by suppression of apoptosis, inflammation, and fibrosis via activating Nrf2/HO-1 pathway.

Keywords:

• Wogonoside
• myocardial ischemia/reperfusion injury
• apoptosis
• inflammation
• fibrosis
• Nrf2/HO-1 pathway

Author contributions

Bingshan Zhang and Di Xu participated in conception of this study. Bingshan Zhang and Di Xu contributed to data analysis and interpretation of the results. Bingshan Zhang wrote this manuscript. Di Xu provided administrative support. All authors approved the final manuscript and agreed to its publication.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

All data generated during this study are included in this article.