A new perspective on the pleiotropic blood pressure improvement effect of sitagliptin: downregulation of miRNA-155 and miRNA-21.

Introduction: Deterioration of vascular responses is the crucial event in the initiation of cardiovascular problems in hypertension (HT) and diabetes mellitus (DM). A well-known oral antidiabetic, sitagliptin, has pleiotropic effects besides improving glycemic state in type-2 DM. This study aimed to investigate the therapeutic effect of sitagliptin on blood pressure with previously unassessed parameters of well-known pathophysiological processes and especially at the microRNA (miRNA) level where there are many unknowns.

The effects of melatonin against atherosclerosis-induced endothelial dysfunction and inflammation in hypercholesterolemic rats.

The aim of this study was to investigate the effects of melatonin on the serum asymmetric dimethylarginine (ADMA) levels and the expressions of vaspin, visfatin, dimethylarginine dimethylaminohydrolase (DDAH), and signal transducer and activator of transcription-3 (STAT-3) for evaluation of endothelial function and inflammation in the hypercholesterolemic rats. Rats were divided into 5 groups: (1) control, (2) hypercholesterolaemia, (3) melatonin administrated concurrently with cholesterol diet, (4) melatonin administrated only last 2 weeks and fed with cholesterol diet, (5) atorvastatin administered only last 2 weeks fed with cholesterol diet. Although an increase was observed in the expressions of visfatin and STAT-3 and the serum ADMA levels, the vaspin and DDAH protein expressions were found to decrease with hypercholesterolemic diets.

The investigation of antioxidant and anti-inflammatory potentials of apitherapeutic agents on heart tissues in nitric oxide synthase inhibited rats via Nω-nitro-L-arginine methyl ester.

Background: High blood pressure effects heart and vessels. Development of pathogenesis is the result of oxidative stress. We aimed to investigate the antioxidant effects of propolis, caffeic acid phenethyl ester (CAPE), and pollen on the hearts of rats which chronic nitric oxide synthase (NOS) inhibited through Nω-nitro-L-arginine methyl ester (L-NAME).

The inhibition of apoptosis through myocardial postconditioning by affecting Fas/FasIg signaling through miR139-3p and miR181a-1.

Background And Aim Of The Study: Ischemic postconditioning (PostC) is considered to be one of the strongest mechanisms limiting the extent of myocardial infarction, and reducing ischemia-reperfusion (I/R) injury. I/R-induced myocardial injury results in apoptosis, autophagy, and necrosis. The aim of the present study was to investigate the roles of the necrotic gene cytochrome b-245 beta chain (Cybb); Cybb-related microRNA miR139-3p; the autophagy gene Beclin-1 (Becn1); proapoptotic genes Fas, Faslg and growth arrest and DNA-damage-inducible 45 alpha (Gadd45a); and apoptosis-related microRNA miR181a-1 levels on I/R injury, as well as, the potential protective effects of PostC through this gene and microRNAs.

Ischemic postconditioning reduced myocardial ischemia-reperfusion injury: The roles of melatonin and uncoupling protein 3.

Objective: Protective effects of ischemic postconditioning (PostC) decrease/disappear with age and chronic heart diseases. Similarly, low serum melatonin levels have been reported in the same risk groups. The aims of this study were to investigate the effects of melatonin on the protection of PostC in ischemia-reperfusion (I/R)-induced infarct size and roles of uncoupling protein (UCP) 3, irisin, and nuclear factor kappa B (NFkB) levels.