Qiliqiangxin Capsule Improves Cardiac Function and Attenuates Cardiac Remodeling by Upregulating miR-133a after Myocardial Infarction in Rats

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.

RETRACTED ARTICLE: Bone Marrow Mesenchymal Stem Cell-Derived Exosomal MicroRNA-133a Restrains Myocardial Fibrosis and Epithelial–Mesenchymal Transition in Viral Myocarditis Rats Through Suppressing MAML1

“…and reduces collagen expression [32], as evidenced in another study. CVF equals the ratio of collagen area to the sum of myocardial area and collagen area, and the mean value shows the CVF of the section [33]. This finding is also reported by Wang et al that VMC mice model is successfully constructed by CVB3 infection, manifesting apparent higher CVF expression in contrast with the control group [34].…”

“…In vitro excessive expression of miR-133a depresses cardiomyocyte hypertrophy and reduces collagen expression [ 32 ], as evidenced in another study. CVF equals the ratio of collagen area to the sum of myocardial area and collagen area, and the mean value shows the CVF of the section [ 33 ]. This finding is also reported by Wang et al .…”

Luhong Granules Prevent Ventricular Remodelling after Myocardial Infarction by Reducing the Metabolites TMAO and LPS of the Intestinal Flora

“…We established an AMI model, a well-characterized animal model of myocardial fibrosis. Myocardial infarction was induced according to a procedure previously described in the literature and adopted in our laboratory [18]. We observed that the induction of myocardial infarction increased the levels of TMAO and LPS, ultimately leading to myocardial fibrosis.…”

Qili Qiangxin Capsule Combined With Sacubitril/Valsartan for HFrEF: A Systematic Review and Meta-Analysis

“…It can enhance the viability of cardiomyocytes by preventing the influx of calcium ions ( Ma et al, 2013 ). Moreover, QQC can block the biological effect of TGF- β 1 and inhibit the intermyocardial fibrosis, delaying or inhibiting ventricular remodeling ( Chen et al, 2019 ).…”