FANG Huan-song, LIU You-zhang, QIU Jun, et al. Effect of Sijunzi Tang on Proteonomics of Myocardial Tissues In Rats With Chronic Heart Failure[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(5): 152-156.
FANG Huan-song, LIU You-zhang, QIU Jun, et al. Effect of Sijunzi Tang on Proteonomics of Myocardial Tissues In Rats With Chronic Heart Failure[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(5): 152-156. DOI: 10.13422/j.cnki.syfjx.2017050152.
Objective: To discuss the effect of Sijunzi Tang on the expression of myocardial proteins in rats with chronic heart failure.Method: Establishing Among 42 SD male rats
6 rats were randomly selected as normal group
and the rest 36 rats were used to establish chronic heart failure rat models. After successful modeling
they were divided into Sijunzi Tang high-dose group and low-dose group (11.88
2.97 g·kg-1·d-1) and Captopril group (100 mg·kg-1·d-1). Rats in blank group and model group received administration of the same volume of normal saline
continuous for 1 month. Left ventricular tissues were taken respectively from various groups
and two dimensional gel electrophoresis was used to isolate proteins of cardiac muscle
analyze the differential protein spots and conduct in-gel digestion and mass spectrum identification for the differential protein spots.Result: Compared with the model group
31 proteins had up-regulated expression and 28 proteins had down-regulated expression in Sijunzi Tang group. 8 proteinswhich displayed significant difference were respectably selected in each group (Volume≥1.5) for mass spectrum identification and 4 proteins were identified as follows after integration and duplicate removal:Suclg2 protein and pyruvate dehydrogenase complex related to energy metabolism; myosin light chain 2 related to myocardial contraction function; and serine protease inhibitor A3N related to myocardial cell reconstruction.Conclusion: Sijunzi Tang could regulate the expression of a variety of myocardial proteins in chronic heart failure rats
probably by regulating the energy metabolism
reducing cardiac remodeling and improving systolic function and heart function.