Inflammation plays a crucial role in the development of many complex diseases and disorders including autoimmune diseases, metabolic syndrome, neurodegenerative diseases, and cardiovascular pathologies. Prostaglandins play a regulatory role in inflammation. Cyclooxygenases are the main mediators of inflammation by catalyzing the initial step of arachidonic acid metabolism and prostaglandin synthesis. The differential expression of the constitutive isoform COX-1 and the inducible isoform COX-2, and the finding that COX-1 is the major form expressed in the gastro-intestinal tract, lead to the search for COX-2-selective inhibitors as anti-inflammatory agents that might diminish the gastrointestinal side effects of traditional non-steroidal anti-inflamatory drugs (NSAIDs). COX-2 isoform is expressed predominantly in inflammatory cells and decidedly upregulated in chronic and acute inflammations, becoming a critical target for many pharmacological inhibitors. COX-2 selective inhibitors happen to show equivalent efficacy with that of conventional NSAIDs, but they have reduced gastrointestinal side effects. This review would elucidate the most recent findings on selective COX-2 inhibition and their relevance to human pathology, concretely in inflammatory pathologies characterized by a prolonged pro-inflammatory status, including autoimmune diseases, metabolic syndrome, obesity, atherosclerosis, neurodegenerative diseases, chronic obstructive pulmonary disease, arthritis, chronic inflammatory bowel disease and cardiovascular pathologies.

Training increases the levels of proteins related to mitochondrial biogenesis and improves the antioxidant capabilities of mitochondria in PBMCs among well-trained football players. Acute exercise may act as an inducer of mitochondrial biogenesis through NF-κB activation and PGC1α gene expression.

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Chronic and non-healing wounds, especially diabetic foot ulcers and radiation injuries, imply remarkable morbidity with a significant effect on the quality of life and a high sanitary cost. The management of these wounds requires complex actions such as surgical debris, antibiotic treatment, dressings and even revascularization. These wounds are characterized by poor oxygen supply resulting in inadequate oxygenation of the affected tissue. The adjuvant treatment with hyperbaric oxygen therapy (HBOT) may increase tissue oxygenation favoring the healing of wounds which do not respond to the usual clinical care. The increase in the partial pressure of oxygen contributes to cover the energy demands necessary for the healing process and reduces the incidence of infections. Moreover, the increase in oxygen leads to the production of reactive species with hormetic activity, acting on signaling pathways that modulate the synthesis of inflammation mediators, antioxidants and growth factors which can contribute to the healing process. Studies performed with cell cultures and in animal models seem to demonstrate the beneficial effects of HBOT. However, clinical trials do not show such conclusive results; thus, additional randomized placebo-controlled studies are necessary to determine the real efficacy of HBOT and the mechanism of action for various types of wounds.