The cardioprotective effects of acteoside in myocardial ischemia reperfusion injury and the underlying mechanism.

INTRODUCTION

We observed the cardioprotective effects of Acteoside (AC) on myocardial ischemia reperfusion injury (MIRI) and discussed the possible mechanisms.

METHODS

Before MIRI model was established successfully, AC was administrated to SD rats by gastric route for 7 d. Punctuate paw withdrawal threshold (PWT) was recorded to reflect the pain threshold. Blood samples were collected to measure the levels of oxidative stress, myocardial enzymes and Norepinephrine (NE). Hematoxylin and eosin (HE) staining was performed to observe the pathological changes of myocardial tissues. Apoptosis of myocardial cell was determined by transferase-mediated dUTP nick end labeling (TUNEL) assay, and the expressions of Bcl-2 and Bax were determined by Western blotting. Using network pharmacological analysis, the PI3K/Akt signaling pathway was screened to be associated with both AC and MIRI. Subsequently, the expressions of PI3K, p-Akt and caspase-3 were detected by immunochemistry in myocardial tissues.

RESULTS

We found that pre-administration of AC improved pain threshold and pathological change of myocardial structure caused by MIRI. AC reduced serum levels of myocardial enzymes and NE in MIRI. Compared with the Sham group, rats in MIRI group showed enhanced oxidative stress levels. These changes were partly reversed by AC. In addition, AC inhibited apoptosis, regulated the expression of apoptosis-related proteins. Immunochemistry analysis confirmed that AC increased the expressions of PI3K and p-Akt in myocardial tissue.

CONCLUSION

The cardioprotective effects of AC in MIRI were related with pain alleviation, oxidative stress, apoptosis and sympathetic nerve activity inhibition, the PI3K/Akt signal pathway activation.

CLINICAL TRIAL NUMBER: Not applicable.