The Role Of Apelin-13 On Quinoline Acid-induced Brain Injury In Mice

In 1993, a new G protein-coupled receptors, named APJ, was discovered by homology cloning. Prior to 1998, it was an orphan receptor, and its endogenous ligand apelin by reverse pharmacology method was screened out. Since the APJ receptor "deorphaning", more and more people have focused on the apelin and APJ receptor system, which have a widespread distribution in both the central nervous system and the periphery. Apelin-APJ system has proved to have many physiological and pathophysiological functions, including the cardiovascular system caused the most concern, lipid and glucose metabolism, fluid balance, as well as immune regulation. However, the neuroprotective potential for them is relatively little concern.We use quinolinic acid (QA) to cause excitatory brain injury in the hippocampus and striatum of Kunming mice, and detect the role of apelin-13 in this mice injury by hematoxylin staining. Our study found that:(1) the micro-injection of lnmol QA to the mouse hippocampus, the dorsal hippocampus CA1 area can cause significantly damage, such as, cells loss and cell shrinkage phenomenon, however, this damage can not be improved by co-injection of both high doses of apelin-13 (5nmol)and lnmol QA. (2) it can produce significant damage to micro-injection of 13nmol QA to the mouse striatal, and through co-injection lnmol of apelin-13, striatal lesion volume was significantly reduced, but 0.3nmol apelin-13 didn’t produce a protective effect to the injury. Thus, apelin/APJ signaling system is very promising as a source of neuronal survival, and should be further investigated the mechanism of its neuroprotective effect. We expect APJ receptor to become a new target in the therapy of brain injury.