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AIM: To explore the pathophysiological mechanism of subarachnoid haemorrhage (SAH) using cellular oxidative stress mechanisms and inflammation. MATERIAL and METHODS: A total of 20 Wistar Albino rats were divided into two groups, namely sham and SAH. On day 0, 0.3 mL of saline in the sham group and 0.3 ml of autologous blood in the SAH group were applied in the cisterna magna of the animals. After sacrification on the 7th day of the procedure, brain, blood and heart tissues were collected. In different tissues, total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), creatin kinase MB (CKMB) and lactate dehydrogenase (LDH) levels were detected biochemically. AKT, sirtuin-1 (SIRT-1), NF-E2–related factor 2 (NRF2), heme oxygenase-1 (HO-1) genes and glutathione peroxidase-4 expression were examined genetically. Moreover, histopathological analyses were conducted both in heart and brain tissues. RESULTS: Enhanced TOS, OSI levels in all tissues and glial fibrillary acidic protein (GFAP) expressions in brain tissue and NFkβ, IL-6 and Cox-1 expressions in heart tissues; it was observed that levels of TAS in blood and AKT, SIRT-1, NRF2 and HO-1 gene expressions in brain tissue were decreased. CONCLUSION: In the oxidative stress and inflammation situation that takes place following SAH, AKT, SIRT-1, NRF2 and HO-1 pathways, which are antioxidant mechanisms, are suppressed and GFAP, NFkβ, IL-6, Cox-1 expressions, which trigger inflammation, are enhanced. Treatment of SAH necessitates studies on the inhibition or activation of such pathways. |
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