Postoperative Cognitive Dysfunction (POCD) is a common central nervous system complication in elderly patients after anesthesia and surgery, characterized by multidimensional cognitive decline, which significantly prolongs hospital stays and increases medical and social burdens. In recent years, the inhalational anesthetic sevoflurane has been widely confirmed as one of the important inducing factors of POCD. This article systematically reviews the strategies for constructing animal models of sevoflurane-induced POCD and its multi-mechanism pathways, focusing on mechanism analysis from six dimensions: neuroinflammation, mitochondrial dysfunction, synaptic plasticity impairment, tau protein phosphorylation, abnormal epigenetic regulation, and changes in blood-brain barrier permeability. Research evidence shows that sevoflurane can induce cognitive impairment by activating microglia, upregulating pro-inflammatory factors (such as IL-6, TNF-α, IL-1β), inhibiting mitochondrial complex Ⅰ/Ⅲ function, inducing oxidative stress, disrupting the expression of synaptic structural proteins, promoting excessive phosphorylation of tau protein, inducing hypermethylation of promoters of key genes such as BDNF, and histone deacetylation. In addition, sevoflurane can damage the integrity of the blood-brain barrier under specific pathological conditions, exacerbating the infiltration of peripheral inflammatory factors into the central nervous system, forming a positive feedback loop between neuroinflammation and cognitive impairment.Sevoflurane induces POCD through a synergistic network of multiple pathways. Future strategies should shift from single-target to multi-pathway interventions to safeguard postoperative cognition in elderly patients.