Carvacrol and Thymol Attenuate Cytotoxicity Induced by Amyloid β(25-35 )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 Aβ in rodent models of AD. In this study, the neuroprotective effects of carvacrol and thymol against Aβ(25-35)-induced cytotoxicity were evaluated, and the potential mechanisms were determined. METHODS: PC12 cells were pretreated with Aβ(25-35) for 2 h, followed by incubation with carvacrol or thymol for additional 48 h. Cell viability was measured by the MTT method. A flurospectrophotometer was employed to observe the intracellular ROS production. PKC activity was analyzed using ELISA. RESULTS: Our results indicated that carvacrol and thymol could significantly protect PC12 cells against Aβ(25-35)-induced cytotoxicity. Furthermore, Aβ(25-35 )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 Aβ(25–35)-induced cytotoxicity in PC12 cells. The results suggested that the neuroprotective effects of these compounds against Aβ(25-35) 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.