Ameliorative effects of osthole on acrylamide-induced neurotoxicity in PC12 cells: Role of oxidative stress, apoptosis and ERK pathways.

The possible protective effects of osthole on acrylamide-induced neurotoxicity in PC12 cells. Cells were pretreated with different concentrations of osthole (1- 25 μM) for 24 h and then the IC₅₀ value of acrylamide (5 mM) was added. After 24 h, cell viability and intracellular ROS content were detected by MTT assay and DCF-DA methods, respectively. Also, DNA fragmentation in apoptotic cells was determined by propidium iodide assay, and apoptosis (Caspase-3, Bax, Bcl-2, ERK, and P-ERK) was measured by the western blot method. Exposing PC12 cells to acrylamide diminished cell viability, and enhanced the intracellular ROS generation and the percentage of apoptotic cells. Furthermore, acrylamide elevated the P-ERK/ERK and Bax/Bcl-2 ratio, and the level of cleaved caspase-3 protein in PC12 cells. Pretreating cells with osthole enhanced cell viability and reduced ROS generation. Also, osthole (10 μM) significantly reduced P-ERK/ERK and Bax/Bcl-2 ratio, the level of cleaved caspase-3 protein, and the percentage of apoptotic cells in comparison to the acrylamide group. Osthole can exhibit a protective effect on the neurotoxicity of acrylamide through the inhibition of oxidative stress and apoptosis in PC12 cells.