Protective Effects of Paeonia lactiflora and Its Active Compound, Paeoniflorin, against Neuronal Oxidative Stress in H_2O_2-Treated SH-SY5Y Cells

Background: Hydrogen peroxide (H_2O_2), a major risk factor of neuronal oxidative stress, initiates a cascade of neuronal cell death. The purpose of this study is to investigate the neuroprotective effects and mechanisms of Paeonia lactiflora (PL) and its active compound, paeoniflorin (PF), against oxidative stress. Methods: Cell viability, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) production, and apoptosis-related protein expression were observed using H_2O_2-induced SH-SY5Y neuronal cells. Results: Treatment with 300 μM H_2O_2 induced cell loss, LDH release, ROS production, and nuclei condensation as shown through Hoechst 33342 staining in SH-SY5Y cells. However, PL and PF treatments significantly diminished neuronal cell death, LDH release, ROS production, and the number of apoptotic cell body. Furthermore, our data showed that treatment with PL and PF significantly attenuated H_2O_2-induced neuronal apoptosis by down-regulating the expression of cleaved caspase-9, caspase- 3, and poly (ADP-ribose) polymerase. The expression of B-cell lymphoma 2/B-cell lymphoma 2-associated X was up-regulated, and PF (10 μg/mL) showed the strongest protective activity against neuronal oxidative stress. Conclusion: Taken together, PL shows to be a promising agent for protection against oxidative stress-related apoptotic neuronal cell death, and its effects were attributed to PF, a major compound of PL.