Abstract: Objective To explore the influence and mechanism of dihydrolycorine ( DL) onrats with viral myocarditis (VMC) induced by Coxsackie B3 virus (CVB3). Methods A total of72 SD rats were randomized into 6 groups: blank control group, model group, 10 mg / kg DLgroup, 20 mg / kg DL group, 40 mg / kg DL group, and Shenmai injection group (200 mg / kg),with 12 rats in each group. The CVB3-induced VMC model was established and intervened for 7days. The levels of serum myocardial enzymes and the hemodynamic indexes were detected. HE staining was used to detect the myocardial tissue pathological damage. TUNEL was used to detect myocardial cell apoptosis. Western blotting was applied to detect the expression levels of apoptosis andendoplasmic reticulum stress-related proteins. Results Compared with those in the model group,the pathological damage of myocardial tissue was alleviated, and the levels of serum myoglobin(Mb), creatine kinase isoenzyme MB (CK-MB) and cardiac troponin I (cTnI), the myocardialapoptosis rate and the protein expression levels of BCL2-associated X protein (Bax), C / EBP homologous protein (CHOP), glucose-regulated protein 78 ( GRP78) and GRP94 were reduced inthe 20 and 40 mg / kg DL groups and the Shenmai injection group ( P < 0. 05). Moreover, the leftventricular pressure (LVP), the maximum change rate of left ventricular pressure rise and fall ( ±dp / dtmax), and the protein expression levels of B-cell lymphoma-2 ( Bcl-2) and the cleaved /caspase-3 ratio rose in the 20 and 40 mg / kg DL groups and the Shenmai injection group ( P <0. 05). Conclusion DL can relieve the VMC myocardial injury and improve the cardiac dysfunction, which may be related to the inhibition of endoplasmic reticulum stress-mediated apoptosis.

Key words: dihydrolycorine, endoplasmic reticulum stress, viral myocarditis, myocardial injury, coxsackie B3 virus, apoptosis