Analysis of microRNA Expression Profiles Induced by Yiqifumai Injection in Rats with Chronic Heart Failure

Abstract

Background: Yiqifumai Injection (YQFM) is clinically used to treat various cardiovascular diseases including chronic heart failure (CHF). The efficacy of YQFM for treating heart failure has been suggested, but the mechanism of action for pharmacological effects of YQFM is unclear.Methods: Echocardiography detection, left ventricular intubation evaluation, histopathology and immunohistochemical examination were performed in CHF rats to evaluate the cardioprotective effect of YQFM. Rat miRNA microarray and bioinformatics analysis were employed to investigate the differentially expressed microRNAs. In vitro models of AngII-induced hypertrophy and t-BHP induced oxidative stress in H9c2 myocardial cells were used to validate the anti-hypertrophy and anti-apoptosis effects of YQFM. Measurement of cell surface area, ATP content and cell viability, Real-time PCR and Western blot were performed.Results: YQFM significantly improved the cardiac function of CHF rats by increasing left ventricular ejection fraction and fractional shortening, decreasing left ventricular internal diameter and enhancing cardiac output. Seven microRNAs which have a reversible regulation by YQFM treatment were found. Among them, miR-21-3p and miR-542-3p are related to myocardial hypertrophy and cell proliferation, respectively and were further verified by RT-PCR. Target gene network was established and potential related signaling pathways were predicted. YQFM could significantly alleviate AngII induced hypertrophy in cellular model. It also significantly increased cell viabilities and ATP content in t-BHP induced apoptotic cell model. Western blot analysis showed that YQFM could increase the phosphorylation of Akt.Conclusion: Our findings provided scientific evidence to uncover the mechanism of action of YQFM on miRNAs regulation against CHF by miRNA expression profile technology. The results indicated that YQFM has a potential effect on alleviate cardiac hypertrophy and apoptosis in chronic heart failure.

Combined detection of miR-21-5p, miR-30a-3p, miR-30a-5p, miR-155-5p, miR-216a and miR-217 for screening of early heart failure diseases

“…In combination with other researchers 'statistics on sample size, we selected more than 60 healthy samples and more than 60 cases of heart failure. Exhaustion samples were analyzed [21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38]. As shown in Figure 1, the aim of the present study was to identify circulating miRNAs in human plasma as biomarkers for the diagnosis of heart failure and its related diseases, to assess the appropriate biomarkers for identifying key characteristics of miRNAs, and to analyze their performance.…”

Effect of modified Wenyang Buxin decoction and routine therapy on cardiac function and serum levels of H-FABP, cTnI and Ang-2 in chronic heart failure patients

“…Therefore, reducing Ang-2 level is beneficial to protecting the myocardial function of the patient. In the study by Zhao et al, renal pathological changes in CHF rats treated with Salvia miltiorrhiza were mitigated [16]. This is because Salvia miltiorrhiza inhibited the expression of angiotensin-converting enzyme and reduced Ang-2 mRNA level, thereby reducing activity of Ang-2.…”

Whole Transcriptomic Analysis of Key Genes and Signaling Pathways in Endogenous ARDS

“…Furthermore, Xiao et al [ 26 ] reported the upregulation of miR-21-3p expression in lung tissue of adult mouse asthma models, which highly correlated with the level of asthma-promoting Th2 cytokines in mouse bronchoalveolar lavage fluid. In addition, in many studies, it has been confirmed that the expression of miR-21-3p in patients with chronic heart failure and pulmonary infection complications or those with severe acute pancreatitis with lung injury complications was higher than that of patients with simple chronic heart failure or severe acute pancreatitis [ 27 , 28 ]. This increased expression of miR-21-3p suggested that lung infection or lung injury might lead to the up-regulation of miR-21-3p.…”