Association between Nfr2, HO-1, NF-kB Expression, Plasma ADMA, and Oxidative Stress in Metabolic Syndrome.

Endothelial dysfunction is one of the major factors in the pathogenesis of metabolic syndrome (MetS), and its molecular mechanisms are not completely understood. The present study aimed to examine the connection between nuclear factor2-related factor2 (Nrf2), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), heme oxygenase 1 (HO-1), and plasma asymmetric dimethylarginine (ADMA) and malondialdehyde (MDA) in people with MetS. Participants in the study were as follows: with MetS ( = 30) and without MetS (Control) ( = 14).

Effect of melatonin on the gastric antioxidant defence in experimental burn trauma.

Severe burn trauma triggers oxidative gastric mucosal injury. The purpose of this study was to investigate the antioxidant defence mechanisms and protective effect of melatonin in the gastric mucosa after burn injury. In order to investigate the mechanisms involved in the gastric antioxidant defence in a rat burn model, quantitative real-time PCR and immunohistochemistry techniques were applied.

Molecular Mechanisms of Melatonin Protection from Gastric Mucosal Apoptotic Injury in Experimental Burns.

Melatonin, a basic secretory pineal gland product, is a nontoxic, multifunctional molecule. It has antioxidant and anti-apoptotic activities and protects tissues from injury. The objective of the present study was to determine the molecular mechanism of melatonin anti-apoptotic effect on gastric injury in a rat burn model.

Molecular mechanisms associating oxidative stress with endothelial dysfunction in the development of various vascular complications in diabetes mellitus.

Endothelial dysfunction plays a key role in the pathogenesis of microangiopathy and macroangiopathy in type 2 diabetes mellitus. The endothelial dysfunction is induced by some cell metabolism disorders which are implicated in the pathogenesis of micro- and macroangiopathies through the principal mediation of oxidative stress. The discussion focuses preferentially on the recently found molecular mechanisms of free radical generation and on the endothelial disorders resulting from some free-radical-induced abnormalities in the intracellular signal pathways.