INTRODUCTON: Alzheimer disease (AD) is a neurodegenerative disorder characterized by a progressive loss of cognitive function. This study aimed to investigate the protective effect of vitamin K2 on toxicity and oxidative damage induced by H2O2 in PC12 cells as an appropriate model similar to Alzheimer's cell damages. Methods: PC12 cells were pretreated with vitamin K2 (5, 10, 20, 50 µM) for 24h and then exposed to H2O2 (150 µM) for 24h. At the end, the cell survival, intracellular reactive oxygen species (ROS) production assessed by analysis of cell viability, ROS generation also the anti-apoptotic effects of vitamin K2 in PC12 cells were studied using flow cytometry after PI staining. Results: Vitamin K2 (5, 10, 20, 50 µM) could decrease H2O2 (150 µM) toxicity and showed significant difference compared to the H2O2 group (***p<0.001). After exposure of cells to H2O2 (150 µM) for 24 h, Vitamin K2 (5, 10, 20, 50 µM) significantly decreased ROS (***P<0.001). Cell apoptosis was significantly increased to 22.6% after treatment with H2O2 (150 µM) compared to control (8%). After pretreatment with vitamin K2 (20, 50 μM); however, apoptosis was significantly reduced to (10.3%, 11.9%). Discussion and Conclusions: Our study revealed that Vitamin K2 may exhibit protective effect on the apoptosis induced by H2O2 in PC12 cells, possibly by reducing oxidative stress. Thus, vitamin K2 may be considered as a valuable candidate drug for the treatment of AD.

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