Objective: The present study was designed to investigate the neuroprotective potential of nebivolol, a β1 adrenergic blocker on aluminium-induced neurobehavioral and biochemical alterations in rats.
Methods: The neurotoxicity was induced by administration of aluminium (50 mg/kg/day, p.o.) for 5 weeks. Nebivolol was administered at a dose of 10 mg/kg, p.o. for 5 weeks. Behavioral assessments were done by using open field test and modified elevated plus maze (mEPM) test. At the end of the study, oxidative stress parameters were determined and histopathological studies of cerebral cortex of rat brains were performed.
Results: Aluminium chloride treated rats showed significant reduction in motor activity in open field test and memory impairment in mEPM test as compared to control group. Nebivolol significantly reversed these parameters and restored brain antioxidant defensive enzymes with reduction in lipid peroxidation. The neurotoxicity was confirmed by the histopathological analysis of cerebral cortex of rat brains. Aluminium treated animals showed presence of ghost cells, vacuolated cytoplasm and haemorrhage in rat cerebral cortex, indicating neurotoxicity. Nebivolol attenuated all these changes. Thus, the potential of nebivolol to prevent aluminium-induced neurotoxicity was also reflected at microscopic level, indicative of its neuroprotective effects.
Conclusion: Nebivolol showed significant antioxidant and neuroprotective activities against aluminium-induced neuronal degeneration. The results of the present study strengthen oxidative stress hypothesis of aluminium-induced neurotoxicity and suggest beneficial role of nebivolol in the treatment of neurodegenerative disorders
