Abstract
Qishen granules (QSG) have beneficial therapeutic effects for heart failure, but the effects of decomposed recipes, including Wenyang Yiqi Huoxue (WYH) and Qingre Jiedu (QJ), are not clear. In this study, the efficacy of WYH and QJ on heart failure is evaluated by using transverse aortic constriction (TAC) induced mice and the significantly changed genes in heart tissues were screened with a DNA array. Furthermore, a new quantitative pathway analysis tool is developed to evaluate the differences of pathways in different groups and to identify the pharmacological contributions of the decomposed recipes. Finally, the related genes in the significantly changed pathways are verified by a real-time polymerase chain reaction and a Western blot. Our data show that both QJ and WYH improve the left ventricular ejection fraction, which explain their contributions to protect against heart failure. In the energy metabolism, QJ achieves the therapeutic effects of QSG through nicotinamide nucleotide transhydrogenase (Nnt)-mediated mechanisms. In ventricular remodeling and inflammation reactions, QJ and WYH undertake the therapeutic effects through 5′-nucleotidase ecto (Nt5e)-mediated mechanisms. Together, QJ and WYH constitute the therapeutic effects of QSG and play important roles in myocardial energy metabolism and inflammation, which can exert therapeutic effects for heart failure.
Highlights
As an incurable and progressive disease, heart failure (HF) has high morbidity and mortality rates in most countries including China [1]
Myocardial hypertrophy plays an important role in heart failure and is an abnormal enlargement of the heart muscle in response to a chronic increase in cardiac workload, which is commonly caused by physiological conditions, such as the amount of exercise performed by an athlete, or pathological disturbances, such as complications of hypertension, valvular heart disease, and other cardiovascular diseases [5]
By decomposing Qishen granules (QSG) into Qingre Jiedu (QJ) and Wenyang Yiqi Huoxue (WYH), we looked to explore the molecular mechanism of the decomposed recipes in the treatment of heart failure
Summary
As an incurable and progressive disease, heart failure (HF) has high morbidity and mortality rates in most countries including China [1]. Molecules 2018, 23, 1829 hypertrophy, the activation of intracellular signaling pathways, and the release of neurohumoral factors; left ventricular (LV) systolic function is still preserved [4]. Ventricular remodeling-induced myocardial hypertrophy is a complex pathophysiologic process characterized by changes in the cellular (tissue) and molecular levels. These changes result in cardiac dilatation and the deterioration of left ventricle (LV) function and they contribute to the development of heart failure [6]. Relatively little is known about the regulation of pathways and molecular events as well as the time-dependent activation during the onset of heart failure and the progression of HF development [7,8,9]. Strategies that prevent and reverse myocardial hypertrophy have attracted attention due to the rising cost of this health burden [10]
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