Abstract
Myocardial apoptosis and fibrosis represent important contributing factors for development of hypertension-induced heart failure. The present study aims to investigate the potential effects of Eriobotrya japonica leaf extract (EJLE) against hypertension-induced cardiac apoptosis and fibrosis in spontaneously hypertensive rats (SHRs). Twelve-week-old male rats were randomly divided into four different groups; control Wistar Kyoto (WKY) rats, hypertensive SHR rats, SHR rats treated with a low dose (100 mg/kg body weight) of EJLE and SHR rats treated with a high dose (300 mg/kg body weight) of EJLE. Animals were acclimatized for 4 weeks and thereafter were gastric fed for 8 weeks with two doses of EJLE per week. The rats were then euthanized following cardiac functional analysis by echocardiography. The cardiac tissue sections were examined by Terminal Deoxynucleotidyl Transferase-Mediated Deoxyuridine Triphosphate (dUTP) Nick End-Labeling (TUNEL) assay, histological staining and Western blotting to assess the cardio-protective effects of EJ in SHR animals. Echocardiographic measurements provided convincing evidence to support the ability of EJ to ameliorate crucial cardiac functional characteristics. Furthermore, our results reveal that supplementation of EJLE effectively attenuated cardiac apoptosis and fibrosis and also enhanced cell survival in hypertensive SHR hearts. Thus, the present study concludes that EJLE potentially provides cardio-protective effects against hypertension-induced cardiac apoptosis and fibrosis in SHR animals.
Highlights
The occurrence of hypertension is increasing rapidly; as a consequence, heart failure (HF) resulting from hypertension has emerged to be a major public health concern [1]
It could be envisaged that the protective effects of Eriobotrya japonica leaf extract (EJLE) against cardiac apoptosis are through attenuation of apoptosis together with enhancement of the survival pathway
The considerable reduction of collagen accumulation and fibrosis associated proteins type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA) in spontaneously hypertensive rats (SHRs) animals through supplementation of EJLE potentially supports their efficacy against hypertension-induced fibrosis in model animals
Summary
The occurrence of hypertension is increasing rapidly; as a consequence, heart failure (HF) resulting from hypertension has emerged to be a major public health concern [1]. Myocardial apoptosis, fibrosis and contractile dysfunction has been implicated as contributing factors for the maladaptive cardiac remodeling process [2]. The pro-apoptotic protein Bad leads to disruption of mitochondrial membrane potential and release of apoptotic factors such as cytochrome c to cytoplasm The release of these factors subsequently initiates a cascade of events eventually leading to apoptosis. Akt appears to be the most important; phosphorylation of Akt at Ser473 residue activates the Akt kinase and initiates the signaling cascade that regulates the expression of pro-survival mediators [12]. Cardiac fibrosis represents another important contributing factor of the maladaptive cardiac remodeling process.
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