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Objective:To assess the effects of Qishen Granule(芪参颗粒, QSG) on sarcoplasmic reticulum(SR) Ca~(2+) handling in heart failure(HF) model of rats and to explore the underlying molecular mechanisms. Methods:HF rat models were induced by left anterior descending coronary artery ligation surgery and high-fat diet feeding. Rats were randomly divided into sham(n=10), model(n=10), QSG(n=12, 2.2 g/kg daily) and metoprolol groups(n=12, 10.5 mg/kg daily). The therapeutic effects of QSG were evaluated by echocardiography and blood lipid testing. Intracellular Ca~(2+) concentration and sarco-endoplasmic reticulum ATPase 2a(SERCA2a) activity were detected by specific assay kits. Expressions of the critical regulators in SR Ca~(2+) handling were evaluated by Western blot and real-time quantitative polymerase chain reaction. Results:HF model of rats developed ventricular remodeling accompanied with calcium overload and defective Ca~(2+) releaseuptake cycling in cardiomyocytes. Treatment with QSG improved contractive function, attenuated ventricular remodeling and reduced the basal intracellular Ca~(2+) level. QSG prevented defective Ca~(2+) leak by attenuating hyperphosphorylation of ryanodine receptor 2, inhibiting expression of protein kinase A and up-regulating transcriptional expression of protein phosphatase 1. QSG also restored Ca~(2+) uptake by up-regulating expression and activity of SERCA2 a and promoting phosphorylation of phospholamban. Conclusion:QSG restored SR Ca~(2+)cycling in HF rats and served as an ideal alternative drug for treating HF.
Objective: To assess the effects of Qishen Granule (sGs) on sarcoplasmic reticulum (SR) Ca2 (2+) handling in heart failure (HF) model of rats and to explore the underlying molecular mechanisms. Methods: HF rat models were induced by left anterior descending coronary artery ligation surgery and high-fat diet feeding. The rats were randomly divided into sham (n = 10), model (n = 10), QSG (n = 12, 2.2 g / kg daily) and The therapeutic effects of QSG were evaluated by echocardiography and blood lipid testing. Intracellular Ca ~ (2+) concentration and sarco-endoplasmic reticulum ATPase 2a (SERCA2a) activity were detected by specific assay kits. Expressions of the critical regulators in SR Ca ~ (2+) handling were evaluated by Western blot and real-time quantitative polymerase chain reaction. Results: HF model of rats developed ventricular remodeling accompanied with calcium overload and defective Ca ~ ( 2+) releaseuptake cycling in cardiomyocytes. Treatment with QS G improved contractive function, attenuated ventricular remodeling and reduced the basal intracellular Ca ~ (2+) level. QSG rapid defective Ca ~ (2+) leak by attenuating hyperphosphorylation of ryanodine receptor 2, inhibiting expression of protein kinase A and up-regulating transcriptional expression of protein phosphatase 1. QSG also restored Ca ~ (2+) uptake by up-regulating expression and activity of SERCA2 a and promoting phosphorylation of phospholamban. Conclusion: QSG restored SR Ca ~ (2+) cycling in HF rats and served as an ideal alternative drug for treating HF.