Riboflavin Bioenriched Soymilk Alleviates Oxidative Stress Mediated Liver Injury, Intestinal Inflammation, and Gut Microbiota Modification in B 2 Depletion-Repletion Mice.

Epidemiological evidence emphasizes that ariboflavinosis can lead to oxidative stress, which in turn may mediate the initiation and progression of liver injury and intestinal inflammation. Although vitamin B 2 has gained worldwide attention for its antioxidant defense, the relationship between B 2 status, oxidative stress, inflammatory response, and intestinal homeostasis remains indistinct. Herein, we developed a B 2 depletion-repletion BALB/c mice model to investigate the ameliorative effects of B 2 bioenriched fermented soymilk (B 2 FS) on ariboflavinosis, accompanied by oxidative stress, inflammation, and gut microbiota modulation in response to B 2 deficiency. In vivo results revealed that the phenotypic ariboflavinosis symptoms, growth rate, EGRAC status, and hepatic function reverted to normal after B 2 FS supplementation. B 2 FS significantly elevated CAT, SOD, T-AOC, and compromised MDA levels in the serum, simultaneously up-regulated Nrf2, CAT, and SOD2, and down-regulated Keap1 gene in the colon. The histopathological characteristics revealed significant alleviation in the liver and intestinal inflammation, confirmed by the downregulation of inflammatory (IL-1β and IL-6) and nuclear transcription (NF-κB) factors after B 2 FS supplementation. B 2 FS also increased the abundance and diversity of gut microbiota, increased the relative abundance of Prevotella and Absiella , as well as decreased Proteobacteria , Fusobacteria , Synergistetes , and Cyanobacteria in strong conjunction with antioxidant, anti-inflammatory properties, and gut homeostasis along with the remarkable increase in cecal SCFAs content. We hereby reveal that B 2 FS can effectively alleviate deleterious ariboflavinosis associated with oxidative stress mediated liver injury, chronic intestinal inflammation, and gut dysbiosis in the B 2 depletion-repletion mice model via activation of the Nrf2 signaling pathway.