Neuroprotective Effects of Aqueous Extract of <i>Bryophyllum pinnatum</i> Against Lead Acetate Induced Damage in the Cerebellum of Rats

Lead is a persistent environmental toxin with pronounced neurotoxic effects, particularly on the central nervous system. This study evaluated the impact of lead acetate on the cerebellar cortex of adult Wistar rats and assessed the neuroprotective effects of aqueous Bryophyllum pinnatum extract. Twenty adult Wistar rats (180–220 g) were randomly assigned to four groups (n = 5): Control (distilled water), T1 (0.075 mg/kg lead acetate), T2 (100 mg/kg B. pinnatum), and T3 (lead + B. pinnatum). Treatments were administered orally for 21 days. Cerebellar tissues were processed for biochemical and histological analysis, and data were analyzed using GraphPad Prism v10.1.Lead exposure significantly decreased body weight and cerebellar weight compared to control (p < 0.01). Superoxide dismutase (SOD) and catalase (CAT) activities were markedly reduced (p < 0.0001), while malondialdehyde (MDA) levels were significantly elevated (p < 0.0001), indicating increased lipid peroxidation. Purkinje cell counts were significantly diminished in the lead-treated group (p < 0.0001). Histologically, lead induced marked neuronal shrinkage, pyknotic nuclei, and cytoplasmic vacuolation in Purkinje cells. Co-treatment with B. pinnatum significantly improved body and cerebellar weights (p < 0.01), restored SOD and CAT activities (p < 0.001), reduced MDA levels (p < 0.0001), and preserved Purkinje neuron morphology and population (p < 0.0001). These results demonstrate that lead acetate induces cerebellar neurotoxicity via oxidative stress mechanisms. B. pinnatum extract effectively mitigates these effects by enhancing antioxidant defense, reducing lipid peroxidation, and maintaining neuronal integrity, underscoring its therapeutic potential against lead-induced neurotoxicity.