Abstract
Inflammatory process has a fundamental role in the pathogenesis of Alzheimer's disease and insoluble amyloid beta deposits and neurofibrillary tangles provide the obvious stimuli for inflammation. The present study demonstrate the effect of pretreatment of 1,8-cineole (Cin) on inflammation induced by A beta((25-35)) in differentiated PC12 cells. The cells were treated with Cin at different doses for 24 h and then replaced by media containing A beta((25-35)) for another 24 h. The cell viability was decreased in A beta((25-35)) treated cells which was significantly restored by Cin pretreatment. Cin successfully reduced the mitochondrial membrane potential, ROS and NO levels in A beta((25-35)) treated cells. Cin also lowered the levels of proinflammatory cytokines TNF-alpha, IL-1 beta and IL-6 in A beta((25-35)) treated cells. Moreover, Cin also succeeded in lowering the expression of NOS-2, COX-2 and NF-kappa B. This study suggests the protective effects of Cin on inflammation and provides additional evidence for its potential beneficial use in therapy as an anti-inflammatory agent in neurodegenerative disease.