Increased SIRT1 Signalling and VEGF Expressions by Dexpanthenol Suppress Oxidant, Inflammatory and Apoptotic Processes in a Rat Experimental Model of Subarachnoid Haemorrhage.

Aim: To investigate the effects of dexpanthenol (Dex) on subarachnoid haemorrhage (SAH) induced brain injury via sirtuin 1 (SIRT1) signaling in a rat experimental model.

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, sham, and DEX 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 analysis as total antioxidant level (TAS), total oxidant level (TOS), 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-?, apoptotic Cas-3, p53, Bax expressions enhanced and antioxidant 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. With the Dex treatment, a decrease was observed in the elevated oxidative, inflammatory, and apoptotic markers. Additionally, antioxidant, anti-apoptotic, VEGF, and SIRT1 levels, showed an increase.

Conclusion: SAH caused inflammation, oxidative stress and apoptosis with decreasing levels of SIRT1 signaling and Dex treatment ameliorated and improved all these pathological conditions.