Background　As a commonly used volatile anesthetics, sevoflurane has been widely used for general anesthesia in clinic. In recent years, many studies have shown that postconditioning with sevoflurane can protect cerebral tissue from ischemia/reperfusion injury but the underlying mechanism is complicated, mainly includes enhancing tolerance of brain tissue to ischemia/reperfusion (I/R), reducing cerebral infarction volume and cerebral edema, reducing oxidative stress and inflammatory response of brain cells, and inhibiting apoptosis of brain cells. Among various mechanisms, inhibition of cell apoptosis plays a key role in the protective effect.　Objective　Summarizing the signal transduction pathway of cell apoptosis that related to the neuroprotection of postconditioning with sevoflurane.　Content　This study reviewed the neuroprotective effect of sevoflurane postconditioning and its regulation on signal transduction about mitochondria-associated and endoplasmic reticulum stress(ERS)-associated apoptosis.　Trend　To better understand the molecular mechanism of neuroprotection of sevoflurane postconditioning and provide a guidance for treatment of patients with cerebral I/R.