Oxidative stress is proved to play an important role in the pathogenesis of Alzheimer's disease (AD). The protective effect of anthocyanin against endogenous Aβ was investigated in N2a/Swe.△9 cells, which are widely used as AD model cells. Anthocyanin belongs to the family of flavonoids extracted from plants. It was demonstrated that anthocyanin at 100 μmol/L significantly inhibited the oxidative stress by decreasing the vulnerability, intracellular ROS and [NO]_i in N2a/Swe.△9 cells. Oxidative stress induces increased activation of C-JunN-terminal kinase (JNK). It was demonstrated that anthocyanin can decrease the activation of JNK in N2a/Swe.△9 cells, suggesting that anthocyanin exerts its protective effect by inhibiting the activation of JNK. Therefore, anthocyanin could act as an oxidative stress suppressor in protecting the N2a/Swe.△9 cells against Aβ induced cell injury and it is a promising candidate for AD treatment in the future.