Centella asiatica extract protects against amyloid β(1–40)-induced neurotoxicity in neuronal cells by activating the antioxidative defence system

Centella asiatica (雷公根 léi gōng gēn) is a traditional medicinal herb with high antioxidant activity, which decreases amyloid-β (Aβ) deposition in the brain. At the same time, aggregated Aβ-induced oxidative stress is the trigger in the pathogenesis of Alzheimer's disease (AD). Here, we investigated the ability of C. asiatica ethanol extract (CAE) to protect PC12 and IMR32 cells from Aβ(1–40)-induced production of reactive oxygen species (ROS) and concomitant neurotoxicity. Aggregated Aβ(1–40) treatment resulted in reduced cell viability, which can be reversed by cotreatment with 25, 50, and 100 μg/mL CAE. Moreover, CAE eliminated the Aβ(1–40)-mediated increase in ROS production. Thus, CAE-mediated protection against aggregated Aβ(1–40)-induced neurotoxicity is attributable to modulation of the antioxidative defense system in cells, including the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and levels of glutathione and glutathione disulfide by CAE. This emphasizes the potential therapeutic and preventive value of CAE in the treatment of AD.