Why the study?
Tongguan Capsule is safe and efficient in ischemic heart diseases, but whether Tongguan capsule derived-herb (TGD) mitigates left ventricular remodeling, dysfunction, and arrhythmias post-MI was unknown.
Does Tongguan capsule derived-herb (TGD) mitigate left ventricular remodeling and reduce arrhythmias in post-myocardial infarction rats?
Does Tongguan capsule derived-herb (TGD) mitigate left ventricular remodeling and reduce arrhythmias in post-myocardial infarction rats?
In a rat model of myocardial infarction, Tongguan capsule derived-herb ameliorated left ventricular remodeling and reduced vulnerability to tachyarrhythmias.
Hypothesis-generating for TGD in post-MI arrhythmia prevention; leaves open translation to human therapy.
OBJECTIVE: Tongguan Capsule, a traditional Chinese medicine, is safe to use and is efficient in treating ischemic heart diseases. The present study aimed to investigate whether Tongguan capsule derived-herb (TGD) can mitigate left ventricular remodeling and dysfunction in post myocardial infarction (MI) rats as well as reduce arrhythmias. DESIGN AND METHODS: MI was induced by a ligation of the left anterior descending coronary artery. TGD was administered to the post-MI rats over a period of 4 weeks. TGD treatment significantly attenuated tachyarrhythmia inducibility and cardiac dysfunction in post-MI heart. Echocardiogram showed that TGD significantly reduced the development of ventricular remodeling. Histological study revealed that TGD significantly reduced myocardial interstitial collagen deposition, myocyte area and α-smooth muscle actin (α-SMA) expression, and increased connexin 43 expression in the infarcted border zone (IBZ). Western blotting results revealed that TGD treatment significantly down-regulated the protein expression levels of type I and III collagen, α-SMA, and up-regulated connexin 43. RT-qPCR results showed that TGD decreased the levels of ANP and BNP. CONCLUSIONS: These findings provided strong evidences that TGD intervention ameliorated interstitial fibrosis, myocyte hypertrophy and gap junction expression in the IBZ, attenuated left ventricular remodeling and dysfunction, and reduced vulnerability to tachyarrhythmia. TGD inhibited IBZ remodeling by its inhibition effect on myofibroblasts differentiation.
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Ma et al. (2019) studied this question.
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