Vitamin K2 Prevents Beta Amyloid Peptide and Vitamin K3‐induced Cell Death

Objective Previous reports have shown that vitamin K2 could prevent oxidative stress‐induced cell death in neuronal and glial cells in vitro (Sakaue et al., 2011; Li et al., 2003). In addition, it has also been reported that there may be a vitamin K deficiency in Alzheimer's patients (Presse et al., 2008). Methods Rat embryo hippocampal astrocytes and neurons were obtained from Brainbits, Inc (Springfield, IL) Inc. and grown on poly‐lysine coated tissue culture‐treated plastic. Neuronal cells were grown for at least eight days in NbActive media (Brainbits, Inc.). The identity of the astrocytes and neurons were confirmed by immunofluorescence using antibodies against GFAP, and synaptophysin respectively. The concentration of β‐amyloid that was used in this study was 10 μM. The concentrations of vitamin K3 and K2 ranged from 1 μM to 100 μM. Cell viability was assessed using the LIVE/DEAD cell imaging kit and lipid peroxidation using the Image‐iT lipid peroxidation kit. Apoptosis was examined via the Magic Red Caspase‐3/7 kit. Results As previously reported, we confirmed that concentrations of 10 uM of vitamin K3 caused an increase in lipid peroxidation and apoptosis in rat astrocytes. On the other hand, concentrations of up to 100 μm of vitamin K2 did not induce lipid peroxidation or apoptosis in either astrocytes or neurons. While neurons treated with β‐amyloid induced apoptosis, when co‐incubated with vitamin K2, there was no apparent neuronal cell death. Co‐incubation of vitamin K2 did also appear to protect astrocytes from vitamin K3 induced damage at the 4 and 24 hour time points as well. Conclusion We report here that vitamin K2 appears to be protective against oxidative stress induced either by beta amyloid or vitamin K3 in both rat astrocytes and neurons. Support or Funding Information A. T. Still University