ANTI-APOPTOTIC EFFECTS OF CHLORELLA VULGARIS AGAINST ALUMINUM CHLORIDE-INDUCED NEUROTOXICITY IN RATS

Aluminum is known to accelerate oxidative stress, mitochondrial damage, and the activation of caspase enzymes, which are key mediators of apoptosis in rat brains. The green microalga Chlorella vulgaris (C. vulgaris) is said to possess neuroprotective properties, reduce inflammation, and have antioxidant qualities. However, their role in aluminum chloride (AlCl3)-induced apoptosis has not yet been fully elucidated. The goal of the current study is to investigate the neuroprotective effects of C. vulgaris in rats after aluminum-induced neurotoxicity through anti-apoptotic and antioxidant mechanisms. Adult male rats were randomly divided into three (3) groups, with 7 animals in each group. Group I administered distilled water; Group II, 100 mg per kilogram body weight of AlCl3; and Group III, 100 mg per kilogram body weight of AlCl3 + 100 mg/ kg C. vulgaris. The trial lasted 60 days, and the oral route of administration was used throughout. The pro-apoptotic protein BAX's expression levels were markedly enhanced by AlCl3 exposure, while those of the anti-apoptotic protein Bcl-2 were dramatically decreased, and Caspase-3 activity was boosted. Additionally, AlCl3 caused GSH levels to drop and MDA levels to rise noticeably. However, treatment with C. vulgaris modulated these oxidative and apoptotic markers via restoration of MDA and GSH levels, as well as the expression levels of BAX, Caspase-3, and Bcl-2 in the brains of rats. According to our findings, C. vulgaris may have therapeutic benefits against aluminum-induced cell death because of its anti-apoptotic and antioxidant properties.