Abstract
particular, in the late-onset formsofAD,epigenetic alterationsmight play an important role in the pathophysiology of this disorder. The sulfur compound and dietary supplement S-adenosylmethionine (SAM) has been reported to have cytoprotective and antioxidant properties in the treatment ofAD.However, the underlyingmechanisms thatmayexplain the cellularprotective effects arenot fully understood.Methods: H 2O 2 -induced neuronal toxicity was characterized in SH-SY5Y human neuroblastoma cells by the decrease of cell viability using PrestoBlue assay (Invitrogen) and by the increase o f intracellular reactive oxygenspecies (ROS) level usingDCFH-DA(2’, 7’-dichlorodihydrofluorescin diacetate) assays.Hemeoxygenase-1mRNAexpressionwas assayedbyRT-PCR. The immunoblotting analysis is implicated for detecting phosphor-c-Jun, phosphor-AKT, andphosphor-ERK1/2 expression to check if the anti-apoptotic signal pathways could be activated by H 2 O 2 medium.Results: Pretreatment with0.01mg/mlSAMsignificantly suppressed theH2O2-inducedelevationof intracellular reactive oxygen species (ROS) level by100%and increased the cell viability by 10%after 24 hours treatment ofH 2O2 adding. Heme oxygenase-1 (HO-1)genewasup-regulatedbut phosphor-AKTwas inhibitedbypretreatment of 0.01 mg/ml SAM. Conclusions: Our results indicated that SAM may activate HO-1 gene expression to perform the protective effect on neuron through the signal of modulating the phospholation of AKT pathway. The epigenetic alterations on gene expression of SAM treatment may explain that provide a dietary supplement of SAMwill be an important part of the interface between the environment and the regulation of gene expression in neuron protection.
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