The Study Of SFN Protects PCl2Cells Against Oxidative Toxicity Through Nrf2-ARE Pathyways

Background:The mechanisms of causing secondary brain damage after stroke are involved in the inflammatory response, radical oxidative damage, and neuronal apoptosis, and oxidative stress is one of the important mechanisms of secondary brain injury. As a two-phase enzyme inducer, SFN has many biological protective effects such as strong anti-oxidative damage, cleared by the group, the anti-apoptosis, which has become the hotspot of the mμLtiple areas of research.SFN can play a cytoprotective effect by activating the Nrf2-ARE pathway. In this paper, we detected cell viability, the rate of apoptosis and expression of Nrf2-ARE pathway targeting protein after SFN intervention on the basis of establishing oxidative damage model by oxidative stress loss of PC12cells induced by MPP+. The effect of Nrf2-ARE pathway on the oxidative stress injury of PC12cells induced by MPP+has been rarely reported. It is unknown how SFN antagonizes oxidative stress injury of PC12cells induced by MPP+by activating the Nrf2-ARE pathway. The aim of the study is to discuss the mechanism of protective effects of SFN in PC12cells, and provide a new idea about cerebral protection and treatment of brain injury.Objective:To investigate the effect and the possible mechanism of SFN on oxidative damage of PC12cells induced by MPP+in vitro.Methods:The oxidative damage model was established by oxidative stress loss of PC12cells induced by MPP+. The cell growth in each group was observed after adding SFN (0.5,1,2.5,5,10μmol/L). Subsequent experiments were divided into four groups:(A) control group,(B) SFN pretreatment Group,(C) MPP+injury group,(D) SFN pretreatment and MPP+injury group. The changes of cell viability, rates of apoptosis and expression of Nrf2, HO-1, NQO1in each group were detected by MTT methods, FCM and western blotting after the PC12cells were incubated with SFN(2.5μmol/L)and/or MPP+(500μmol/L) for24h in vitro.ResμLts:Compared with group A, the viability of PC12cells was significantly decreased in MPP+-treated groups (100to700μmol/L). The neurotoxic effect of MPP+were significantly decreased by SFN pretreatment, when the cells were co-incubated with MPP+and different concentrations of SFN pretreatment for24h. SFN pretreatment group cell survival had improved significantly. Compared with control group, the rate of apoptosis was increasing in MPP+group. But the rate of apoptosis were significantly decreasing after pretreatment of the SFN. Compared with MPP+group, the expression of Nrf2, HO-1and NQO1protein were increasing significantly in SFN pretreatment group.Conclusion:SFN had a protective effect against damage by MPP+-induced in PC12cell, which may be performed by activating Nrf2-ARE pathway.