Catalpol attenuates the neurotoxicity induced by beta-amyloid(1-42) in cortical neuron-glia cultures.

A glia-mediated inflammation plays an important role in the pathogenesis of Alzheimer's disease (AD). In vitro, besides a direct neurotoxic effect on neurons, Abeta activates glia to produce an array of inflammatory factors including tumor necrosis factor-alpha (TNF-alpha), reactive oxygen species (ROS), nitric oxide (NO) and inducible nitric oxide synthase (iNOS), which accelerate the progression of AD. Catalpol, an iridoid glycoside, isolated from the root of Rehmannia glutinosa, protects neuronal cells from damage caused by a variety of toxic stimulus. In the present study, the effect of catalpol against Abeta(1-42)-induced neurotoxicity in primary cortical neuron-glia cultures as well as its mechanism acting on cells was further investigated. Pretreatment with catalpol at the dosage of 500 microM for 30 min prior to 5 microM Abeta(1-42) not only attenuated the Abeta(1-42)-triggered neurotoxicity to neurons but also inhibited the glial activation to some extent, which was examined by inspecting the morphological changes and measuring the release of the above mentioned inflammatory factors. Therefore, the results demonstrated that catalpol might be a promising anti-inflammatory agent in the therapy or prevention of neurodegenerative diseases associated with inflammation.