Abstract
Qiliqiangxin capsule (QLC), a natural herb recipe with therapeutic effect from China, has been widely used in clinical practice for attenuating cardiac remodeling induced by myocardial infarction (MI). However, the pharmacological mechanism of QLC on cardiac remodeling after MI is not entirely clear. The present study aims to investigate the effectiveness and mechanisms of QLC on cardiac remodeling induced by MI in rats. The animal model was established by permanently ligating the left anterior descending coronary artery in rats. Subsequently, rats with successful ligation were randomly divided into model group, captopril group, and QLC group. And the control group was operated upon in parallel except ligation, namely, the sham group. All rats were treated through the intragastric administration once a day for 4 weeks. Cardiac hemodynamics was measured after treatment. Then, the left ventricular mass index (LVMI) was examined. The pathological changes were observed by HE staining. The collagen volume fraction (CVF) was detected by Masson trichrome staining. The apoptosis index was obtained by TUNEL fluorescent staining. The miR-133a and mRNA of TGF-β1, CTGF, Caspase9, and Caspase3 were examined by real-time PCR. The protein expressions of TGF-β1, CTGF, Caspase9, Caspase3, and cleaved-Caspase3 were tested by Western blot. Compared with the model group, QLC partially improved cardiac hemodynamics and decreased LVMI. miR-133a was significantly increased in QLC group. In addition, QLC declined CVF by downregulating TGF-β1 rather than CTGF. Meanwhile, QLC decreased the apoptosis index by attenuating Caspase9, Caspase3, and cleaved-Caspase3. This study suggested that QLC could improve cardiac function and partially attenuate cardiac remodeling by attenuating fibrosis and decreasing apoptosis, which might be partially related to miR-133a, TGF-β1, Caspase9, and Caspase3.
Highlights
Coronary heart disease is considered as one cardiovascular disease (CVD) seriously affecting human health worldwide, which may develop into myocardial infarction (MI) or even chronic heart failure
Cardiac remodeling after MI is a complex pathophysiological process that seriously threatens the patient's life, which includes inflammation, fibrosis, apoptosis, and other pathological processes. These pathological factors contribute to the development of heart failure after MI, which indicate that it is positive to mitigate the adverse impact as soon as possible [13]
In China, Traditional Chinese medicine (TCM) have been considered as an alternative and adjuvant approach to the prevention of CVD and injury induced by ischemia/reperfusion [8, 14, 15]
Summary
Coronary heart disease is considered as one cardiovascular disease (CVD) seriously affecting human health worldwide, which may develop into myocardial infarction (MI) or even chronic heart failure. Cardiac remodeling after MI involves complex pathological changes, which cause cardiac dysfunction [2]. With the continuous exploration of pathological mechanism, people gradually realized the important roles of miRNAs in cardiac remodeling after MI [3, 4]. MiR-133a seemed to a central role in the diagnosis and the treatment of cardiac remodeling [6, 7]. Traditional Chinese medicine (TCM) has long been widely applied to treat CVD [8]. Whether its therapeutic mechanisms are related to miR-133a is a meaningful issue worthy of attention and discussion. At the same time, according to the TargetScan database (online database for predicting miRNA target genes), TGF-β1, CTGF, Caspase, and Caspase might be downstream genes of miR-133a, and their changes deserved our attention
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