To investigate the neuroprotective effects and mechanisms of Maresin 2 (Mar2) in the early stage of subarachnoid hemorrhage (SAH) in mice. Methods: A total of 134 male C57BL/6 mice were randomly divided into Sham group (12 mice), Vehicle group (22 mice), Mar2 group (57 mice), Tau group (29 mice), and Tau+Mar2 group (14 mice), with the Mar2 group further divided into low (2 μg/kg/d; 14 mice), middle (10 μg/kg/d; 29 mice), and high (50 μg/kg/d; 14 mice) dose subgroups. The SAH model was prepared using a modified intravascular perforation method, and Mar2 was injected intraperitoneally 6 hours after SAH modeling; the Tau group received an intraperitoneal injection of Tau at a dose of 0.5 g/kg/d for 3 consecutive days; the Tau+Mar2 group received an intraperitoneal injection of Tau followed by a middle dose of Mar2 2 hours later. After the injections, neurological function scores, cerebral hemorrhage scores, and brain tissue water content were measured for each group of mice. FJB staining was used to assess the number of degenerating neurons, immunofluorescence staining was used to observe changes in the number of astrocytes and microglia, Western blotting was used to detect the expression of endoplasmic reticulum stress protein C/EBP homologous protein (CHOP) and caspase-3 in neurons, and quantitative PCR (qPCR) was used to detect changes in the inflammatory cytokines interleukin-1β (IL-1β) and IL-6 in brain tissue. In vitro cultured Neuro2a neurons were treated with heme or taurine sodium cholate (Tau, CHOP-specific inhibitor), and divided into control group, Hem group, Hem+Tau group, and Hem+Tau+Mar2 group. Western blotting was used to detect the levels of CHOP and caspase-3 expression in neurons; enzyme-linked immunosorbent assay was used to measure ROS levels. Results: Mar2 injection significantly improved neurological deficits, reduced brain edema, inhibited neuronal apoptosis, and a middle dose (10 μg/ kg/d) achieved the best therapeutic effect. Western blotting results showed that Mar2 could inhibit the expression of CHOP and caspase-3 in the cortex; immunofluorescence staining results showed that Mar2 could inhibit the activation and increase of astrocytes and microglia; qPCR detection results showed that Mar2 injection could significantly reduce the expression of inflammatory cytokines IL-1β and IL-6. In vitro experiments showed that heme could induce significant upregulation of CHOP and caspase-3 in neurons and increase the synthesis of ROS; Mar2 treatment could significantly inhibit the expression of CHOP and caspase-3 in neurons. High-dose Tau treatment could significantly inhibit the expression of CHOP and caspase-3 in neurons, and Tau +Mar2 treatment could not further reduce the expression of CHOP and caspase-3. Conclusion: Mar2 injection can inhibit neuronal apoptosis in SAH mice, reduce brain edema, and improve neurological deficits. The specific mechanism may be related to Mar2 inhibiting the activation of neuronal CHOP, downregulating the expression of caspase-3, and reducing neuroinflammation.