Objective: To investigate the effects of baicalin on ventricular remodeling

ventricular myocyte apoptosis and β1-adrenoceptor(β1-AR)/protein kinase A (PKA)/Ca2+/calmodulin-dependent priotein kinase Ⅱ (CaMK Ⅱ) signaling pathway in rats with dilated cardiomyopathy induced by adriamycin(ADR). Method: Sixty male Wistar rats were randomly divided into normal group

model group

baicalin low

middle and high dose groups and Carvedilol group. The model group received intraperitoneal injection of ADR 2 mg · kg-1; Baicalin and Carvedilol groups were given with baicalin (25

50

100 mg · kg-1)

carvedilol 10 mg · kg-1 · d-1 gavage on the basis of model group; while the normal group was given with an equal volume of 0.9% NaCl by intraperitoneal injection

1 time/week

for a total of 3 times.At the end of 7 weeks

the ventricular ultrasonography and heart function were measured by ultrasonography. The levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) and human stromelysin-2(ST2)in serum were detected by enzyme-linked immunosorbent assay (ELISA). The apoptosis of ventricular myocytes was observed by TdT-mediated dUTP nick-end labeling(TUNEL) staining. The expression levels of β1-AR

PKAand CaMK Ⅱ in ventricular myocytes were detected by Western blot. Result: As compared with the normal group

the rats in the model group showed obvious ventricular remodeling and decreased cardiac function(P<0.05); the levels of NT-proBNP and ST2 were increased (P<0.05); the number of apoptotic cells was increased (P<0.05)

and the expression levels of β1-AR

PKA and CaMKⅡwere also increased. As compared with the model group

the ventricular remodeling and cardiac function were improved in baicalin and carvedilol groups; the levels of NT-proBNP and ST2 were decreased (P<0.05)

and the number of apoptotic cells was decreased (P<0.05); and the expression levels of β1-AR

PKA and CaMK Ⅱ in ventricular myocardium were also decreased (P<0.05). Conclusion: Baicalin can effectively improve the ventricular remodeling and decrease the apoptosis of cardiomyocytes in ADR-induced dilated cardiomyopathy rats. The mechanism may be related to the inhibition of β1-AR/PKA/CaMK Ⅱ signaling pathway in ventricular myocytes.