Abstract Body: Background: Inflammation and oxidative stress are key drivers of subarachnoid hemorrhage (SAH) pathology, leading to brain injury and vasospasm. This study aimed to evaluate the effects of a lipid emulsion-based oxygen carrier, perfluorocarbon-Oxygent (PFC-Oxygent), as a promising therapeutic agent to limit inflammation and oxidative stress following SAH. PFC-Oxygent consists of lipid emulsion microparticles with high flexibility. Unlike red blood cells, the ultra-small size of these particles allows them to flow even with minimal residual plasma trickle and efficiently deliver oxygen, thereby aiding in the prevention of tissue damage. Methods: Adult C57BL/6 wild-type mice were subjected to the endoperforation model of SAH, followed by intravenous injection of PFC-Oxygent or saline (9ml/kg) at 5 hours post-SAH. At 48 hours post-SAH, the mice were evaluated for functional outcomes. Subsequently, the mice were transcardially perfused, and the brains were harvested for immunohistochemistry and biochemical analyses. Results: SAH induced significant behavioral impairments and triggered NLRP3 inflammasome activation and upregulation of oxidative stress markers at 48h post-SAH. Treatment with PFC-Oxygent, however, attenuated these functional impairments. Notably, the SAH group treated with PFC-Oxygent, showed a significant reduction in NLRP3 inflammasome components and oxidative stress markers. Conclusion: These findings demonstrate that PFC-Oxygent treatment improves functional outcomes and reduces NLRP3 inflammasome-mediated inflammation and oxidative stress following SAH. Overall, these findings underscore the therapeutic potential of PFC-Oxygent treatment in mitigating SAH severity.