Neuroprotective Potential of Thunbergia laurifolia Lindl Leaf Extracts Against Beta Amyloid-induced Neurotoxicity: An in vitroModel of Alzheimer's Disease

Background: Beta-amyloid peptide (A beta) induces oxidative stress, contributing to Alzheimer's disease (AD) initiation and progression. This study aims to explore Thunbergia laurifolia (T. laurifolia) leaf extract's protective effects on A beta 25-35-induced oxidative stress and cell injury in SH-SY5Y cells and investigate underlying mechanisms. Materials and Methods: SH-SY5Y cells were treated with T. laurifolia leaf extract in the presence or absence of A beta 25-35. After 24 h, neuroprotective effects were assessed using cell viability and lactate dehydrogenase (LDH) assays. Caspase-3/7 activity, intracellular reactive oxygen species (ROS) levels, catalase (CAT), and superoxide dismutase (SOD) activities were measured to examine mechanisms. Total flavonoid and phenolic content assays were performed. Results: The findings showed that exposure to A beta 25-35 led to a notable rise in oxidative stress in SH-SY5Y cells, as evidenced by increased levels of ROS. Additionally, A beta 25-35 treatment increased caspase-3/7 activity and LDH release and decreased cell viability. However, T. laurifolia extract effectively suppressed ROS production, attenuated caspase-3/7 activity, and concentration-dependently reduced A beta 25-35-induced neurotoxicity. LDH release decreased, and cell viability increased. SOD and CAT activities also increased after T. laurifolia treatment. The extract had total phenolic and flavonoid contents of 178.5 +/- 6.86 and 32.51 +/- 1.26 mg/g, respectively. Conclusion: T. laurifolia extract demonstrated neuroprotective effects against A beta 25-35-induced injury in SH-SY5Y cells. These effects were attributed to reduced oxidative stress, elevated SOD and CAT activity, and suppressed caspase-3/7 activity. T. laurifolia extract shows potential as an alternative or therapeutic approach to AD mediated by A beta. Nevertheless, further research is needed to elucidate the mechanism by which T. laurifolia ameliorates neuronal cell death induced by A beta 25-35.