Objective To explore the possible mechanism of anti-myocardial ischemia-reperfusion injury of Mongolian medicine E’erdun-Wurile pretreatment. Methods A total of 60 SD rats were randomly divided into sham operation group

model group

Compound Danshen Dropping Pills group and Mongolian medicine high

medium and low dose group

with 10 rats in each group. The Mongolian medicine high

medium

and low-dose groups were given the E’erdun-Wurile suspension respectively at a dose of 1. 2

0. 6

and 0. 3 g/kg each time

while Compound Danshen Dropping Pills group was given compound Danshen Dropping Pill solution at a dose of 0. 5 g/kg each time

and the sham operation group and the model group were given equal volume of distilled water twice daily for 2 weeks. Twelve hours after the last administration

the sham operation group was treated with only the thread not ligated

the other groups were treated with left anterior descending coronary artery ligation to prepare myocardial ischemia-reperfusion injury model. After successful modeling

the pathological changes of myocardial tissue in each group were observed by HE staining. The expressions of autophagy-related proteins Beclin1 and microtubule-associated protein light chian 3 protein Ⅱ（ LC3-Ⅱ） were detected by immunohistochemistry. The Beclin1 and LC3-Ⅱ proteins in myocardial tissue and expression of PI3 K-Akt-mTOR signaling pathway-associated proteins were detected by Western blot. Results Compared with the model group

all medicated drug groups could improve the pathological morphology of rat myocardial tissue. The expressions of LC3-Ⅱ and Beclin1 in the myocardial tissues of the Mongolian medicine middle and high dose groups were lower than those in the model group（ P < 0. 05）

while the relative expression of PI3 K-Aktm TOR signaling pathway in the myocardial tissue was higher than that of the model group（ P < 0. 05）. Conclusion Mongolian medicine E’erdun-Wurile can alleviate myocardial tissue damage in rats with myocardial ischemia-reperfusion injury

which may be related to down-regulation of autophagy-related proteins LC3-Ⅱ and Beclin1 expression and activation of PI3 K-Akt-mTOR signaling pathway.