Riboflavin Bioenriched Soymilk Alleviates Oxidative Stress Mediated Liver Injury, Intestinal Inflammation, and Gut Microbiota Modification in B2 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 (B2FS) on aribotlavinosis, accompanied by oxidative stress, inflammation, and gut microbiota modulation in response to B-2 deficiency. In vivo results revealed that the phenotypic aribotlavinosis symptoms, growth rate, EGRAC status, and hepatic function reverted to normal after B2FS supplementation. B2FS significantly elevated CAT, SOD, T-AOC, and compromised MDA levels in the serum, simultaneously up-regulated Nrf2, CAT, and SOD2, and down-regulated Keapl gene in the colon. The histopathological characteristics revealed significant alleviation in the liver and intestinal inflammation, confirmed by the downregulation of inflammatory (IL-1 beta and IL-6) and nuclear transcription (NF-kappa B) factors after B2FS supplementation. B2FS also increased the abundance and diversity of gut microbiota, increased the relative abundance of Prevotella and Absiclla, as well as decreased Proteobacteria, Fusobacteria, Synergistetes, and Cyanobactcria in strong conjunction with antioxidant, anti-inflammatory properties, and gut homeostasis along with the remarkable increase in cecal SCFAs content. We hereby reveal that B2FS 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.

Automated summary

The study reveals that B2FS can effectively alleviate the detrimental effects of ariboflavinosis, including oxidative stress-mediated liver injury, chronic intestinal inflammation, and gut dysbiosis, through the activation of the Nrf2 signaling pathway in the B-2 depletion-repletion mice model.