Apelin-13 triTFA is the endogenous ligand of the APJ receptor, activating this G protein-coupled receptor with an EC50 value of 0.37 nM.

Apelin-13 highly increased AQP4 expression as well as reduced neurological scores and infarct volume.?Importantly, Apelin-13 played a role of BBB protection in both types of mice by reducing BBB permeability, increased vascular endothelial growth factor, upregulated endothelial nitric oxide synthase, and downregulated inducible NOS. In morphology, we demonstrated Apelin-13 suppressed tight junction opening and endothelial cell swelling via electron microscopy detection.?Meanwhile, Apelin-13 also alleviated apoptosis of astrocytes and promoted angiogenesis[1].?Apelin 13 treatment significantly reduced infarct size, improved neurological outcomes, decreased brain edema, and inhibited cell apoptosis, oxidative stress, and neuroinflammation after I/R. Apelin 13 significantly increased the expression of Nrf2 and the phosphorylation levels of AMPK and GSK-3β[2].

The expression of AQP4 induced by Apelin-13 injection at 1, 3, and 7 days after middle cerebral artery occlusion.?Meanwhile, examined the effects of Apelin-13 on neurological function, infarct volume, and BBB disruption owing to cerebral ischemia in wild type mice, and tested whether such effects were AQP4 dependent by using AQP4 knock-out mice[1].