Protective effects of vitamin K2 on 6-OHDA-induced apoptosis in PC12 cells through modulation bax and caspase-3 activation.

Neuroprotection using compounds with dual functions of anti-apoptotic and antioxidant effects fight against neurodegeneration. Vitamin K2 acts as a cofactor in many biochemical pathways, including sphingolipid synthesis in the nervous system, which is involved in many cellular events, including proliferation, differentiation, cellular communication, and alteration. This study aimed to investigate the protective effects of vitamin K2 in PC12 cells as an in vitro model of Parkinson's disease. The protective effects of vitamin K2 against 6-OHDA-induced apoptosis in PC12 cells were assessed using resazurin for viability, DCF-DA for ROS level, DTNB for glutathione level, flow cytometry for sub G1, and western blot analysis for detecting bax and pro-caspase-3 expression level. The results showed that 6-OHDA significantly decreased cell viability, glutathione and pro-caspase-3 levels, and increased ROS, the amount of bax in PC12 cells, while the pretreatment with 5 μM vitamin K2 significantly decreased the cell death induced by 6-OHDA. Generally, the results may present a new insight about the potential protective action of vitamin K2 against the progression of Parkinson's disease. Further studies may warrant the use of vitamin K2 as an antioxidant and anti-apoptotic agent in slowing nerve injury in neurodegenerative disease, particularly in Parkinson's disease.