Morpho-functional indicators changes of rats’ myocardium in experimental doxorubicin-induced chronic heart failure and its pharmacological modulation with new 4-amino-1,2,4-triazole derivative

Bromide 1 - (β-phenylethyl)-4-amino-1,2,4-triazolium (Hypertril) has the properties of a beta-blocker and of NO-mimetic, is assigned to the IV class of toxicity. All these effects make Hypertril a promising drug for the treatment of cardiovascular diseases. The aim of this paper was to study the cardioprotective action of Hypertril in terms of the effect on the morpho-functional parameters of the myocardium in rats with experimental chronic heart failure (CHF). CHF was modeled on 80 white outbred rats weighing 190–220g by administering doxorubicin at a cumulative dose of 15 mg/kg. Hypertril and the reference drug metoprolol succinate were administered within 30 days after CHF modeling, intragastrically at doses of 3.5 mg/kg and 15 mg/kg. Morphometric analysis of the cellular structure of the myocardium was carried out on an Axioskop microscope (Zeiss, Germany), in an automatic mode using a macro program developed in a specialized programming environment VIDAS-2.5 (Kontron Elektronik, Germany). The administration of Hypertril to animals with CHF led to an increase in the density of nuclei of cardiomyocytes, the area of myocardiocyte nuclei, an increase in the nuclear cytoplasmic ratio and an increase in the concentration of RNA in the nuclei and cytoplasm of cardiomyocytes compared with the group of untreated animals, which indicated the presence of a pronounced cardioprotective effect in the drug candidate. In terms of such indicators as the density of surviving cardiomyocytes and the content of RNA in them, the nuclear-cytoplasmic ratio of Hypertril is significantly (p < 0.05) superior to metoprolol.

Cardioprotective Action of Glycyrrhizin on Diabetic Rats with Myocardial Remodeling

Introduction. Cardiovascular disorders are one of the prominent causes of risks of mortality which accounts for high rate of the deaths at a global level. The risk of deadly myocardial infraction grows because of diabetes which even causes the development of heart failure. Objective. The objective of this study was to understand and study the effect of glycyrrhizin on diabetes suffering rats with myocardial remodeling. Materials and Methods. Streptozotocin was used for induction of diabetes, and 8–12 weeks later, the assessment of inflammation, fibrosis, and cardiac damage was evaluated. Histopathological analysis and immunohistochemistry was performed to analyze the effect in various groups. Western blotting was performed to understand the proteins expressed in diabetes, and also, their expression was noted in treatment groups. Results. There was a significant rise in TNF-α, dense fibrosis, and collagen deposits in the STZ diabetes group. The effects of hyperglycemia were significantly improved in the glycyrrhizin-treated group. DAPI, BrDu, and caspase staining was also performed to understand apoptosis in tissues where the diabetic groups reported significant apoptosis, while the effects were significantly lower in the treated group. Conclusion. All the observations indicate that glycyrrhizin has cardioprotective action in diabetic rats with myocardial remodeling and is due to the inhibition of the NF-κB signaling pathway in the myocardial layer.

Uridine treatment prevents myocardial injury in rat models of acute ischemia and ischemia/reperfusion by activating the mitochondrial ATP-dependent potassium channel

The effect of uridine on the myocardial ischemic and reperfusion injury was investigated. A possible mechanism of its cardioprotective action was established. Two rat models were used: (1) acute myocardial ischemia induced by occlusion of the left coronary artery for 60 min; and (2) myocardial ischemia/reperfusion with 30-min ischemia and 120-min reperfusion. In both models, treatment with uridine (30 mg/kg) prevented a decrease in cell energy supply and in the activity of the antioxidant system, as well as an increase in the level of lipid hydroperoxides and diene conjugates. This led to a reduction of the necrosis zone in the myocardium and disturbances in the heart rhythm. The blocker of the mitochondrial ATP-dependent potassium (mitoKATP) channel 5-hydroxydecanoate limited the positive effects of uridine. The data indicate that the cardioprotective action of uridine may be related to the activation of the mitoKATP channel. Intravenously injected uridine was more rapidly eliminated from the blood in hypoxia than in normoxia, and the level of the mitoKATP channel activator UDP in the myocardium after uridine administration increased. The results suggest that the use of uridine can be a potentially effective approach to the management of cardiovascular diseases.

Cardioprotective action of chia (Salvia hispanica L.) in ovariectomized rats fed a high fat diet

The combination of ovariectomy with high fat diet consumption, in this study, affected biometric parameters, oxidative stress, mineral content and ATPase pump activity, while chia consumption had positive effects on these factors.

Synthesis and cardioprotective effectiveness of arginine succinates

The synthesis was developed and physic-chemical properties of the pharmaceutical substance the di-L-arginine succinate were determined. Its cardioprotective effectiveness in cases of ischemic-reperfusion injury of the myocardium was demonstrated in experiments on rats. The substance was used to obtain the drug Inokardin of cardioprotective action.