Secukinumab Ameliorates Oxidative Damage Induced by Subarachnoid Hemorrhage

Abstract

This study aimed to investigate the histological and biochemical neuroprotective effects of secukinumab (SEC) on brain damage induced by subarachnoid hemorrhage (SAH) in male Wistar Albino rats. Forty male Wistar Albino rats were randomly divided into four groups of equal size: Control, SEC, SAH and SAH+SEC. SAH was induced the SAH and SAH+SEC groups by injecting autologous blood collected from the hearts of the rats into the subarachnoid space via the foramen magnum. SEC was administered intraperitoneally once a week to the SEC and SAH+SEC groups after the surgical procedure. On the 14th day of surgery, the rats were sacrificed and their cerebral tissues were collected for biochemical analysis and histopathological examination. SAH led to changes in oxidative stress parameters by increasing malondialdehyde (MDA) levels and decreasing superoxide dismutase (SOD), glutathione (GSH), catalase (CAT) and glutathione peroxidase (GPx) levels. Histopathologically, cerebral tissues in the SAH groups showed alterations such as congestion and cell infiltration. Treatment with SEC significantly reduced MDA levels and increased SOD, GSH, CAT and GPx levels. SEC also decreased histopathological alterations in brain tissues. This study revealed that SEC (3 mg/kg) therapeutically influenced oxidative and histopathological changes in blood parameters and brain tissues caused by experimental SAH. SEC helps reduce brain damage in rats with SAH and possesses antioxidant and neuroprotective properties. Further advanced studies are needed to prove its potential benefits for humans.