Indian journal of pharmacology · 2026
Rice bran extract ameliorates experimental colitis by modulating gut dysbiosis and toll-like receptor 4/nuclear factor kappa β signaling.
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Shendy Hagar M, Galal Omneya, Wadie Walaa, Abdeltawab Nourtan F, Helal Amr, Khayyal Mohamed T, Mohamed Sarah S
Аннотация
OBJECTIVES: Gut dysbiosis is widely recognized to serve as crucial role in the etiology of inflammatory bowel disease (IBD). This research evaluates the ability of a stabilized rice bran extract (RBE) to modulate positively microbial dysbiosis in an experimentally induced IBD model.
MATERIALS AND METHODS: Rats were given 5% dextran sulfate sodium (DSS) in drinking water during a week to cause colitis. RBE was administered to the rats with a daily dosage of 100 mg/kg, 1 week before feeding them with DSS and continued during DSS treatment. Fecal samples were then collected to assess alterations in the chosen microbial phyla, while colon samples were processed for histological and biochemical assessment.
RESULTS: The colonic expression of toll-like receptor 4 (TLR4), nuclear factor kappa β (NF-κB), tumor necrosis factor alpha, and interlukin-17 (IL-17) was significantly elevated when DSS induced colitis, resulting in significant histopathological damage and a decrease in the amount of IL-10. Furthermore, DSS caused the colonic tight junction (TJ) protiens mRNA expression to drop dramatically. All undesirable changes induced by DSS tended to be reversed by RBE. Moreover, RBE beneficially modulated the gut microbiota by restoring various bacteria to their normal levels.
CONCLUSIONS: The current research demonstrated the potential protective effect of RBE against colonic inflammation through modulating microbiota dysbiosis, TJ protein dysfunction, and TLR4/NF-κB signaling.
MATERIALS AND METHODS: Rats were given 5% dextran sulfate sodium (DSS) in drinking water during a week to cause colitis. RBE was administered to the rats with a daily dosage of 100 mg/kg, 1 week before feeding them with DSS and continued during DSS treatment. Fecal samples were then collected to assess alterations in the chosen microbial phyla, while colon samples were processed for histological and biochemical assessment.
RESULTS: The colonic expression of toll-like receptor 4 (TLR4), nuclear factor kappa β (NF-κB), tumor necrosis factor alpha, and interlukin-17 (IL-17) was significantly elevated when DSS induced colitis, resulting in significant histopathological damage and a decrease in the amount of IL-10. Furthermore, DSS caused the colonic tight junction (TJ) protiens mRNA expression to drop dramatically. All undesirable changes induced by DSS tended to be reversed by RBE. Moreover, RBE beneficially modulated the gut microbiota by restoring various bacteria to their normal levels.
CONCLUSIONS: The current research demonstrated the potential protective effect of RBE against colonic inflammation through modulating microbiota dysbiosis, TJ protein dysfunction, and TLR4/NF-κB signaling.