[[Stroke]] is a significant cardiovascular disease that influences the health of human beings all over the world, especially the elderly population. It is reported that the [[blood-brain barrier]] (BBB) can be easily destroyed by [[stroke]], which is one of the main factors responsible for [[macrophage]] infiltration and central nervous [[inflammation]]. 

Zang et al. reported the protective effects of Trelagliptin against BBB injury and macrophage infiltration. The results indicate that the infraction volume, the neurological score, and macrophage infiltration staining with [[CD68]] were increased in [[middle cerebral artery occlusion]] (MCAO) mice but significantly reversed by treatment with Trelagliptin. Additionally, Trelagliptin reduced the permeability of the BBB by increasing the expression of the tight junction [[zonula occludens protein-1]] (ZO-1) in the cerebral cortex. In an in vitro hypoxia model of endothelial cells, the increased migration of macrophages, enlarged permeability of endothelial monolayer, downregulation of [[ZO-1]], and elevated expression level of [[CXCL1]] by hypoxic conditions were all reversed by treatment with Trelagliptin in a dose-dependent manner. The results demonstrate that Trelagliptin might mitigate macrophage infiltration by preventing the breakdown of the blood-brain barrier in the brains of MCAO mice
((Zang L, Yang B, Zhang M, Cui J, Ma X, Wei L. [[Trelagliptin]] Mitigates [[Macrophage Infiltration]] by Preventing the Breakdown of the [[Blood-Brain Barrier]] in the Brain of [[Middle Cerebral Artery Occlusion]] Mice. Chem Res Toxicol. 2021 Mar 17. doi: 10.1021/acs.chemrestox.0c00323. Epub ahead of print. PMID: 33728903.)).