As the prevalence of
inflammatory bowel diseases (IBD) rises, the etiology of IBD draws increasing attention.
Glucoraphanin (GRP), enriched in cruciferous vegetables, is a precursor of
sulforaphane, known to have anti-inflammatory and antioxidative effects. We hypothesized that dietary GRP supplementation can prevent
mitochondrial dysfunction and oxidative stress in an acute
colitis mouse model induced by
dextran sulfate sodium (DSS). Eight-week-old mice were fed a regular rodent diet either supplemented with or without GRP. After 4 weeks of dietary treatments, half of the mice within each dietary group were subjected to 2.5% DSS treatment to induce
colitis. Dietary GRP decreased DSS-induced
body weight loss, disease activity index, and colon shortening.
Glucoraphanin supplementation protected the colonic histological structure, suppressed inflammatory
cytokines,
interleukin (IL)-1β,
IL-18, and
tumor necrosis factor-α (TNF-α), and reduced macrophage infiltration in colonic tissues. Consistently, dietary GRP activated
AMP-activated protein kinase (AMPK),
peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1α, and nuclear factor erythroid 2-related factor 2 (NRF2) pathways in the colonic tissues of DSS-treated mice, which was associated with increased
mitochondrial DNA and decreased content of the oxidative product
8-hydroxydeoxyguanosine (8-OHDG), a
nucleotide oxidative product of
DNA. In conclusion, dietary GRP attenuated
mitochondrial dysfunction, inflammatory response, and oxidative stress induced by DSS, suggesting that dietary GRP provides a dietary strategy to alleviate IBD symptoms.