Objective: To clarify the protective effect of Linggui Yangxin decoction (LGYXD) on myocardial injury and heart function

and observe the effect of LGYXD on calcium regulation associated protein of myocardial sarcoplasmic reticulum (SR) in rats with Adriamycin-induced dilated cardiomyopathy (DCM)

in order to explore its possible mechanism.Method: A total of 60 SD rats were randomly divided into normal group and DCM group. The latter was further divided into five groups:DCM control

perindopril and LGYXD groups. DCM was induced through intraperitoneal injection with Adriamycin (1.0 mg · kg-1

twice a week) for 6 weeks. The treatment lasted for 8 weeks. At the 9th week

echocardiography and myocardial metabolism imaging were performed on DCM rats to evaluate the efficiency. Serum levels of brain natriuretic peptide (BNP) and cardiac troponin-I (cTnI) were measured by enzyme-linked immunosorbent assay. Cardiac histological changes were examined by hematoxylin and eosin (HE) staining and electron microscopy. The mRNA and protein expressions of sarcoplasmic reticulum Ca2+-ATPase (SERCA2a)

ryanodine receptor (RyR2)

phospholamban (PLB)

Calsequestrin

L-type Ca2+ channel (CAV1.3) in rat hearts from each group were determined by reverse transcription-polymerase chain reaction (RT-PCR) and western blotting.Result: Compared with the DCM control group

LGYXD can improve cardiac cavity size

and alleviate cardiac function

myocardial injury and cardiac histological changes in DCM rats. Compared with the DCM control group

expressions of SERCA2a mRNA

RyR2 mRNA

CAV1.3 mRNA

and Calsequestrin mRNA in myocardial tissues of LGYXD group were increased

and expression of PLB mRNA was decreased. Compared with the DCM control group

the protein expressions of SERCA2a and Calsequestrin of LGYXD group were increased

and the protein expression of PLB was decreased.Conclusion: LGYXD can effectively reduce the dilated left ventricular diameter of DCM rat

improve EF and FS

decrease the serum levels of BNP and cTnI

protect myocardium and improve heart function. LGYXD can partially regulate mRNA and protein expressions of PLB

SERCA2a

RyR2

CAV1.3

Calsequestrin in rats with dilated cardiomyopathy. The mechanism of LGYXD in treating DCM rats may be correlated with the regulation of the mRNA and protein expressions of calcium regulation-associated protein of myocardial sarcoplasmic reticulum in rats with dilated cardiomyopathy

and the improvement of Ca2+ transport function of myocardial cells and systolic-diastolic function of heart.