Aim:Oxidative stress and inflammation occur in the brain after a subarachnoid hemorrhage (SAH) by using some intracellular pathways. Dexpanthenol (Dex) uses these mechanisms and causes antioxidant and anti-inflammatory action. This study aimed to investigate the effects of Dex on SAH induced brain injury via sirtuin1 (SIRT1) signaling.Material and Methods:A total of 46 Wistar Albino rats were divided into 5 groups as control, sham, SAH, SAH+Dex and Dex. First day; 0.3 ml of saline was given to the cisterna magna of the control and sham group animals and 0.3 ml of autologous blood was given to SAH and SAH+Dex. On day 4; brain tissues of the rats were removed under anaesthesia. Brain tissues were collected for the biochemical anaysis as TAS (Total antioxidant level), TOS (Total oxidant level) and oxidative stress index (OSI) levels; histopathological and immunohistochemical analysis as caspase-3 (Cas-3), vascular endothelial growth factor (VEGF); and genetical anaylsis as SIRT1/P53/B-cell lymphoma (BCL2)/Bcl-2-associated X protein (Bax). Results:Oxidant TOS, OSI levels, inflammatory TNF-α, apoptotic Cas-3, P53, Bax expressions enhanced and antioxidan TAS, antipoptotic BCL2, angiogenetic marker VEGF and SIRT1, which affects all these biomarkers decreased in the SAH group significantly. Besides significant subarachnoidal and parenchymal hemorrhage areas, edematous cerebral membranes, degenerative and necrotic changes and neuronophagies were observed. Dex treatment reversed all of these biomarkers.Conclusion:SAH caused inflammation, oxidative stress and apoptosis with decreasing levels of SIRT1 signaling and Dex treatment ameliorated and corrected all these pathological conditions.