Neuroprotective effect of lupeol in animal model of D-galactose induced cognitive dysfunction

Abstract Objective Cognitive dysfunction is common in neurodegenerative diseases and aging, often associated with reduced antioxidant activity and increased brain inflammation. This study aimed to investigate the neuroprotective effects of lupeol, a pentacyclic triterpenoid derived from Emblica officinalis, on oxidative stress and cognitive decline induced by D-galactose in rats. Methods Sprague–Dawley rats were administered D-galactose (100 mg/kg) to induce cognitive dysfunction, followed by lupeol treatment at doses of 10, 25, and 50 mg/kg. Behavioral assessments evaluated learning and memory performance, while biochemical analyses measured glutathione (GSH) peroxidase activity, reactive oxygen species (ROS), nitrite, acetylcholinesterase (AChE) activity, and advanced glycation end products (AGEs) in the cortex and hippocampus. Key findings Lupeol treatment significantly improved learning and memory compared to the D-galactose group. Biochemically, lupeol enhanced GSH activity, reduced ROS and nitrite levels, and decreased AChE activity, reflecting improved cholinergic function. Furthermore, lupeol lowered AGE accumulation, suggesting mitigation of AGE-related neuronal damage. Conclusion Lupeol confers protection against D-galactose-induced neurodegeneration through its antioxidant and anti-inflammatory properties. These findings support lupeol’s potential as a therapeutic agent for age-related cognitive impairments and neurodegenerative disorders.