Postoperative cognitive dysfunction ( POCD) is a prevalent complication affecting the central nervous system following anesthesia and surgery in elderly patients. It is characterized by a multidimensional decline in cognitive function, which significantly extends hospital stays and increases both medical and social burdens. Recent studies have identified the inhalational anesthetic sevoflurane as a significant contributing factor to the onset of POCD. This systematic review considers the strategies used to construct animal models of sevoflurane-induced POCD and explores its multifaceted mechanistic pathways. The analysis focuses on six dimensions: neuroinflammation,mitochondrial dysfunction, synaptic plasticity impairment, tau protein phosphorylation, abnormal epigenetic regulation, and alterations in blood-brain barrier (BBB) permeability. Empirical evidence indicates that sevoflurane can induce cognitive impairment by activating microglia, upregulating pro-inflammatory factors inhibiting mitochondrial complex Ⅰ/ Ⅲ function, inducing oxidative stress, disrupting the expression of synaptic structural proteins, promoting excessive phosphorylation of tau protein, and inducing hypermethylation of promoters of key genes such as brain-derived neurotrophic factor( BDNF), along with histone deacetylation. Furthermore, sevoflurane can compromise the integrity of the BBB under specific pathological conditions, exacerbating the infiltration of peripheral inflammatory factors into the central nervous system and establishing a positive feedback loop between neuroinflammation and cognitive impairment. Sevoflurane induces POCD via a synergistic network involving multiple pathways. Future strategies should transition from single-target to multi-pathway interventions to protect postoperative cognitive function in older adult patients.