SIRT1 attenuated oxidative stress induced by methyl tert-butyl ether in HT22 cells
Methyl tertiary-butyl ether (MTBE), an unleaded gasoline additive, can lead to oxidative stress then injuring nervous system after long-term exposure.SIRT1, a NAD+-dependent histone deacetylase, can play a neuroprotective role in brain injury. However, the mechanism is unclear. This present study intended to define the role of SIRT1 during process of MTBE- induced oxidative stress in mouse hippocampal neurons cells (HT22 cells). Our data showed that MTBE could directly trigger oxidative stress in HT22 cells by decreasing the activieies of superoxide dismutase (SOD) and GSH/T-GSH level, and increasing ROS, lipid peroxidation product malondialdehyde (MDA) and GSSG level. Similarly, the expression of SIRT1, an antioxidant, decreased with the dose-dependent to MTBE. To further explore whether SIRT1 played a key role during the process of oxidative stress, HT22 cells were transfected with siRNA-SIRT1 and preconditioned with agonist of SIRT1 (SRT1720) for 2h, respectively. The levels of oxidative stress (ROS, SOD, MDA, GSH/ GSSG) were detected again after siRNA-SIRT1 HT22 cells and SRT1720 HT22 cells exposure to MTBE for 6 h. In contrast to the non-pretreated group, levels of oxidative stress were tonic in siRNA-SIRT1 HT22 cells and attenuated in SRT1720 HT22 cells. Our resluts indicated that MTBE could directly cause oxidative stress in HT-22 cells and SIRT1 might be an important antioxidant during MTBE induced-oxidative stress.