Half of the daily requirement of Vitamin K2 (menaquinones) is fulfilled by the intestinal microbiota. Menaquinones helps to improve bone-health and prevent coronary calcification. Dysbiosis has been associated with CNS functions via gut-brain axis and involved in the modulation of psychiatric conditions. In the present study we use Vitamin K2 (MK-7) as therapeutics against gut dysbiosis associated cognitive decline.

Gut dysbiosis was induced in mice by administration of Ampicillin (250 mg/kg twice a day orally) for 14 days. Vitamin K2 (100 mcg/kg once a day orally) was administered in another group for 21 days parallel to antibiotic dose of 14 days. Gene expression studies revealed that antibiotic decreased the relative abundance of Lactobacillus, Bifidobacterium, Firmicutes and Clostridium while the levels were restored by Vitamin K2 treatment. Behavioural studies showed cognitive decline using fear conditioning, spatial and recognition memory tests in antibiotic group which were reversed upon Vitamin K2 treatment to antibiotic animals. Vitamin K2 reduced gut dysbiosis mediated increase in myeloperoxidase, an inflammation marker, in colon and brain. Similarly, Vitamin K2 reduced the brain acetylcholine esterase and oxidative stress induced by antibiotic. Vitamin K2 treatment also protected hippocampal neurons and changes in intestinal ultrastructure from gut dysbiosis associated damage as revealed by histopathological studies.

We conclude that Vitamin K2 prevented antibiotic associated gut dysbiosis leading to reduced intestinal and brain inflammation and oxidative stress thus preventing hippocampal neuronal damage and eventually improving the cognitive function.