Ghrelin as an anti-inflammatory and protective agent in ischemia/reperfusion injury

•Ischemia/reperfusion injuries continue to be among the most frequent causes of death and are often associated with microvascular dysfunction.•Ghrelin provides reduction of proinflammatory responses mediating regulation of protein expression involved in ischemia / reperfusion injury.•Immunomodulatory mediators inhibit the release of many proinflammatory factors from immune and non-immune cells promoting tissue regeneration.•Ghrelin is a potential target for therapeutic interventions involved in reducing the extent of oxidative stress and inflammation evoked in IRIs. Ischemia/reperfusion (I/R) continue to be the most frequent cause of damaged tissues. Injured tissues resulted from the first ischemic insult, which is determined by the interruption in the blood supply, followed by subsequent impairment induced by reperfusion. In addition, ischemia-reperfusion injury is mediated by tumor necrosis factor (TNF) and other cytokines that activate complements and proteases responsible for free radical production. However, earlier studies have reported the protective roles of bioactive peptides during ischemia reperfusion injury. In fact, ghrelin is a peptide hormone discovered since 1999 as GH secretagogue and its production was identified in gastric X/A-like endocrine cells in rats and P/D1 type cells in humans. To date, this peptide receives growing attention due to its pleiotropic action in the organism and its role in maintaining energy homeostasis. Ghrelin is also involved in stress responses, assuming a modulatory action on immune pathways. Previous studies have identified many other functions related to an anti-inflammatory role in ischemia reperfusion injury. Under these challenging conditions, studies described acylated and unacylated ghrelin in activation and/or inhibition processes related to ischemia-reperfusion injury. The aim of this article is to provide a minireview about ghrelin mechanisms involved in the proinflammatory response of I/R injury. However, the regulatory processes of ghrelin in this pathologic event are still very limited and warrant further investigation.