Beta carotene provides neuroprotection against amikacin induced toxicity

Abstract

Background and objectives: Beta carotene is a precursor of vitamin A and acts as a potent antioxidant in the body. Beta carotene, as an antioxidant, helps to protect cells from damage caused by these free radicals. This study aimed at investigating the cytoprotection provided by beta carotene against amikacin induced brain damage.Methods: To do so, four groups of animals were used (seven rats in each group): the control group, the amikacin group, the beta carotene with the amikacin group, and the group given beta carotene first, then added amikacin later together with the beta carotene. Results: The results revealed that amikacin has disrupted the brain architecture resulting in vascular congestion, brain oedema, and cellular vacuolization while beta carotene has protected the cells architecture maintain cellular architecture and providing tissue protection in particular in the group were beta carotene has administered before amikacin. Conclusion: Beta-carotene has emerged as a promising therapeutic agent for reducing the neurotoxic effects induced by amikacin. Through histological findings, it has been demonstrated that beta-carotene exerts its protective effects by preserving neuronal integrity, reducing oxidative stress, and modulating neuroinflammatory responses. Further research is warranted to explore the exact mechanisms by which beta-carotene confers neuroprotection and to determine the optimal dosage and duration of treatment. Nonetheless, these findings highlight the potential of beta-carotene as a useful adjunct therapy in the management of amikacin-induced neurotoxicity.