Protective Effect of Cinnamaldehyde on METH-induced Neurotoxicity in PC12 Cells via Inhibition of Apoptotic Response and Oxidative Stress.
Roghayeh Rashidi, Seyed Adel Moallem, Mohammad Moshiri, Farzin Hadizadeh, Leila Etemad
Abstract
-cinnamaldehyde (TCA) on METH-induced cytotoxicity. PC12 cells were treated with METH (2.5 mM) 24 h after treated with different concentrations of TCA (3.75- 50 μM). The percentage of cell survival was evaluated by MTT assay and the following parameters were measured to detect apoptosis and oxidative stress responses: DNA fragmentation, ROS production and GSH content. Exposure to 2.5 mM METH decreased the cell viability and GSH levels, caused the generation of reactive oxygen species and ultimately induced apoptosis. Pretreatment with TCA at 3.125-25 μM significantly attenuated cell viability loss. TCA, especially at a concentration of 12.5 and 25 μM, decreased the apoptosis and ROS generation and increased the GSH level compared with the METH group. The findings of the present study suggested that TCA exerted a protective effect against METH-induced neurotoxicity through mechanisms related to antioxidant and anti-apoptosis. It is suggested that TCA may be useful for the prevention and treatment of harmful effects of METH on the brain.