Ameliorative effect of ferruginol on isoprenaline hydrochloride‐induced myocardial infarction in rats

Abstract

Cardiovascular‐related diseases continue to be a leading cause of death globally. Among ischemic‐induced cardiac diseases, myocardial infarction (MI) is reported to be of an alarming value. Despite numerous improvements in the medical intrusions, still this armamentarium fails to be effective in managing the illness without setbacks. Ferruginol (FGL) is a major polyphenols and terpenoids with numerous pharmacological activities including antioxidant and anti‐inflammatory. Following, this work was aimed to explore the cardio protective effect of FGL (50 mg/kg) in isoprenaline hydrochloride (ISO)‐induced MI in experimental rats. After treatment with FGL in ISO‐induced MI in rats, noticeable changes were observed in the experimental rats. Injection of ISO to rats resulted in the augmented cardiac weight, serum cardiac markers (creatine kinase, creatine kinase‐MB, cardiac troponin T, and Cardiac troponin I), lipid peroxidation end products (thiobarbituric acid‐reactive substance and lipid hydroperoxides), reduced endogenous antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione), reduced ATPase activity, and escalated pro‐inflammatory cytokines (interleukin‐6, tumor necrosis factor‐α, and nuclear factor‐κB) levels. Interestingly, the FGL supplementation to the ISO‐treated rats revealed the diminished heart weight, reduced cardiac markers, and lipid peroxidation. FGL also possessed the improved antioxidants status and diminished pro‐inflammatory mediator levels. The outcomes of histological analysis also evidenced the cardio protective role of FGL. Treatment with FGL reduced the cardiac damage biomarkers maintained to near normal levels in ISO‐induced rats. These study findings disclose the prospective capability of FGL in the treatment of MI in the future.

Effects of a collagen hyaluronic acid silk‐fibroin patch with the electroconductive element polyaniline on left ventricular remodeling in an infarct heart model

“…The COL‐SF group showed higher TBARS concentration when compared to healthy. MI may reduce the activity of antioxidant enzymes, 35,36 explaining the low activity of GPx in all infarcted groups. Zhang and colegahes 35 reported that antioxidant enzymatic activity was induced by increasing ROS concentration.…”

Dynamic Mitochondrial Proteome Under Polyamines Treatment in Cardiac Aging

“…Nicotinamide nucleotide transhydrogenase (NNT, Spd:O = 1.571) is a nuclear gene encoded protein located in the mitochondrial inner membrane, which catalyzes mitochondrial transmembrane hydride transfer between NAD(H) and NAD(P)+ to generate NAD(P)H. It has been demonstrated that the NAD+/NADH ratios affect the activity of the sirtuins family, which are potential mediators of the beneficial effects of calorie restriction and mediating lifespan, and an age-dependent loss of gene expression of NNT which linked to mitochondrial dysfunction ( Olgun, 2009 ). Moreover, NNT increases NADPH level, which is important for antioxidant systems, biosynthesis, aging, and apoptosis ( Zhang et al, 2021 ). NNT overexpression can be used as management strategies to decrease the ratio of NADH/NAD+ and aging.…”

Cardioprotective Effect of Gossypin Against Myocardial Ischemic/Reperfusion in Rats via Alteration of Oxidative Stress, Inflammation and Gut Microbiota

“…Oxidative damage and mitochondrial dysfunction are associated with increased LPO and reduced endogenous antioxidant enzymes in the myocardial tissue. 41 , 42 The enzymatic antioxidant myocardial system works in a coordination manner to maintain the cellular redox balances. During the ISO treatment, a disturbance occurred in the redox balance in the myocardial.…”

“…LPO is a crucial pathogenic process in the condition of cardiac injury and the effect of ISO on LPO in the myocardial tissue of rodents is well established. 41 , 42 The peroxidative injury is exerted through the quinone formation (intermediates of ISO), which reacts with the molecular oxygen to generate the ROS and induces the membrane LPO. 41 In this experimental protocol, gossypin considerably suppressed the ISO mediated TBARS (LPO marker) in myocardial tissue, suggesting a potent antioxidant effect to protect the myocardium.…”

“…38 IL-6 involved in numerous inflammatory reactions such as neutrophil recruitment and maturation. 42 During the cardiac disease, the level of IL-6 increased and it suppressed the catalase activity and enhanced the inflammatory and toxic effects. 38 The results showed that gossypin treatment considerably reduced the levels of IL-6, IL-1β, TNF-α and NF-κB in the heart tissue as well as serum as compared to I/R control group rats, suggesting an anti-inflammatory effect, which protects the heart from I/R injury.…”