Effect of thymol on amyloid β25-35-mediated PC12 cells death by activating protein kinase C and inhibiting oxidative stress

Background and Aim : Despite more than a century of intensive research on AD, few effective treatment options have been developed. Nowadays, several medicinal plants and their constituents have been suggested as possible treatments for AD. In this study, the neuroprotective effect of thymol against Aβ25-35-induced cytotoxicity was evaluated, and the potential mechanisms were determined. In this regards, we investigated whether thymol could inhibit cytotoxicity and oxidative damage caused by Aβ through antioxidant activity and stimulation of protein kinase C (PKC).Methods : PC12 Cells were pretreated with Aβ25-35 for 2 h followed by being incubated with thymol for additional 48 h. Cell viability was measured by MTT method. Flurospectrophotometer was employed to observe intracellular reactive oxygen species (ROS) production. PKC activity was analyzed using ELISA.Results : Our results indicated that, thymol could protect PC12 cells against Aβ25-35-induced cytotoxicity. Furthermore, the results demonstrated that, Aβ25-35 induces intracellular ROS production, while thymol could reverse this effect. Moreover, thymol could elevate PKC activity similar to Bryostatin-1. So, we mainly reported two points: first, thymol could reduce ROS levels in Aβ-treated PC12 cells, and second it might act as a PKC activator.Conclusion : This study provided the evidence regarding the protective effect of thymol against Aβ25–35-induced cytotoxicity in PC12 cells. Also, the results suggested that, neuroprotective effects of this compound against Aβ25-35 might be through attenuating oxidative damage and increasing the activity of PKC as a memory-related protein. Thus, thymol was found to have therapeutic potential in preventing or modulating AD.

Keywords:

Alzheimer’s disease (AD) , amyloid β (Aβ) , thymol , reactive oxygen species (ROS) , protein kinase C (PKC) , PC12 cells