Carvacrol and Thymol Attenuate Cytotoxicity Induced by Amyloid beta25-35 via Activating Protein Kinase C and Inhibiting Oxidative Stress in PC12 Cells.

Background: Our previous findings indicated that carvacrol and thymol alleviate cognitive impairments caused by Abeta in rodent models of Alzheimer's disease (AD). In this study, the neuroprotective effects of carvacrol and thymol against Abeta25-35-induced cytotoxicity were evaluated, and the potential mechanisms were determined. Methods: PC12 cells were pretreated with Abeta25-35 for 2 h, followed by incubation with carvacrol or thymol for additional 48 h. Cell viability was measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method. A flurospectrophotometer was employed to observe the intracellular reactive oxygen species (ROS) production. Protein kinase C (PKC) activity was analyzed using ELISA. Results: Our results indicated that carvacrol and thymol could significantly protect PC12 cells against Abeta25-35-induced cytotoxicity. Furthermore, Abeta25-35 could induce intracellular ROS production, while carvacrol and thymol could reverse this effect. Moreover, our findings showed that carvacrol and thymol elevate PKC activity similar to Bryostatin-1, as a PKC activator. Conclusion: This study provided the evidence regarding the protective effects of carvacrol and thymol against Abeta25-35-induced cytotoxicity in PC12 cells. The results suggested that the neuroprotective effects of these compounds against Abeta25-35 might be through attenuating oxidative damage and increasing the activity of PKC as a memory-related protein. Thus, carvacrol and thymol were found to have therapeutic potential in preventing or modulating AD.