Vitamin K2 protects against D-galactose induced ageing in mice

Ageing is a complex process characterized by the gradual deterioration of physiological functions, often leading to a diminished quality of life. Dementia is among the prominent indicators of ageing characterized by cognitive impairment. Animal studies employing D-galactose have provided insights into the mechanisms underlying cognitive decline and neuronal degeneration, resembling features of human brain ageing while Vitamin K2, known for its diverse physiological functions, also have neuroprotective potential. Here we study the effect of Vitamin K2 in D-galactose induced ageing in mice.

Ageing was induced in adult Swiss albino mice using D-galactose via subcutaneous (SC) route for 45 days while one group of animals received Vitamin K2 (MK-7) via oral gavage during last 21 days. Then different behavioral studies, including the elevated plus maze, Morris water maze, passive avoidance and novel object recognition test were performed to measure cognitive changes, followed by measuring AChE, corticosterone (plasma), oxidative stress parameters (SOD, GSH, MDA) and pro-inflammatory markers (TNFα, IL1β) in hippocampal homogenates. Histopathology of the hippocampal sections were performed to measure neuronal density.

Vitamin K2, treatment reversed D-galactose associated memory changes. In the biochemical studies, plasma corticosterone was reduced while hippocampal AChE, MDA and pro-inflammatory cytokines were reduced after Vitamin K2 treatment. The antioxidants like SOD and GSH were improved in Vitamin K2 treated animal brain. The hippocampal neuronal density increased in treatment group compared to D-galactose induced aged animals.

Treatment with Vitamin K2 (MK-7) partially reversed cognitive decline associated with ageing, highlighting its potential as a therapeutic intervention for age associated cognitive decline.