In recent years, remote ischemic preconditioning is found as a novel way to protect the brain, which may be achieved  through nerve pathways, humoral factors or nerve-humoral interaction. The molecular mechanisms for the protection might be related  to mitochondria ATP-sensitive potassium channel, mitogen-activated protection kinase, mammalian target of rapamycin, including  nitric oxide synthase and cannabinoid receptors. The aim of this review is to explain the mechanism of action of remote ischemic  preconditioning on brain protection, as well as the possible direction of clinical application.