Pharmacological postconditioning: a molecular aspect in ischemic injury

Abstract

Objective Ischaemia/reperfusion (I/R) injury is defined as the damage to the tissue which is caused when blood supply returns to tissue after ischaemia. To protect the ischaemic tissue from irreversible injury, various protective agents have been studied but the benefits have not been clinically applicable due to monotargeting, low potency, late delivery or poor tolerability. Key Findings Strategies involving preconditioning or postconditioning can address the issues related to the failure of protective therapies. In principle, postconditioning (PoCo) is clinically more applicable in the conditions in which there is unannounced ischaemic event. Moreover, PoCo is an attractive beneficial strategy as it can be induced rapidly at the onset of reperfusion via series of brief I/R cycles following a major ischaemic event or it can be induced in a delayed manner. Various pharmacological postconditioning (pPoCo) mechanisms have been investigated systematically. Using different animal models, most of the studies on pPoCo have been carried out preclinically. Summary However, there is a need for the optimization of the clinical protocols to quicken pPoCo clinical translation for future studies. This review summarizes the involvement of various receptors and signalling pathways in the protective mechanisms of pPoCo.

The Role of LincRNA-EPS/Sirt1/Autophagy Pathway in the Neuroprotection Process by Hydrogen against OGD/R-Induced Hippocampal HT22 Cells Injury

“…Interestingly, many studies have also shown that pharmacological preconditioning (PreCo) or postconditioning (PoCo) is beneficial to the ischemic organ. Subsequently, the main advantage of pharmacological PoCo over ischemic preconditioning or pharmacological PreCo is its added clinical feasibility or clinically applicable [47]. CI/R injury is often seen in unannounced clinical situations, such as cardiac arrest or ischemic stroke.…”

Inflammatory Pathogenesis of Post-stroke Depression

“…This immune activation is characterized by the release of signaling molecules from the injured tissue, invoking a potent immune reaction aimed at repairing the damage [19]. Furthermore, adhesion molecules on endothelial cells stimulate circulating white blood cells to adhere to activated endothelial cells, leading to microvascular blockade and the infiltration of immune cells into the brain parenchyma [20].…”

Ischemic Tolerance—A Way to Reduce the Extent of Ischemia–Reperfusion Damage

“…The mechanism of ischemic postconditioning includes activation of the adenosine receptors, α-adrenergic receptors, opioid receptors, and bradykinin, with activation of pathways such as the PKC, TK, and MAP kinase, or the activation mechanism involves an endogenous trigger such as NO and Ca 2+ ions. The administration of drugs whose effect mimics the mechanism of the action of ischemic postconditioning is called pharmacological postconditioning (FAP) [ 138 , 139 ].…”