In mice with a form of intestinal inflammation, phytic acid is linked to lower levels of specific inflammatory signaling molecules in the colon.
Mechanism
Synthesis from 1 study
Phytic acid blocks a cellular switch that normally turns on inflammation in the gut. When this switch is off, the gut cells stop producing too many inflammatory chemicals and keep their protective barrier intact, which stops further irritation from gut bacteria.
Most probable mechanism
Phytic acid enters gut cells and blocks a key signaling pathway that normally turns on inflammation genes. When this pathway is turned off, the cells stop making excessive amounts of inflammatory chemicals like IL-1β, IL-6, and TNF-α. This also helps keep the gut lining sealed and protected, preventing bacteria from triggering more inflammation.
Phytic acid enters intestinal epithelial cells and interacts with intracellular signaling components to inhibit AKT phosphorylation
Reduced AKT activity prevents activation of the IKK complex, which normally triggers degradation of IκBα
IκBα remains intact and binds to NF-κB p65, preventing its translocation into the nucleus
NF-κB p65 cannot bind to DNA, leading to reduced transcription of pro-inflammatory genes including Il-1β, Il-6, and Tnf-α
Lower levels of inflammatory cytokines reduce immune cell activation and preserve expression of tight junction proteins and mucin-2 in the colonic epithelium
Intact epithelial barrier limits bacterial translocation and prevents sustained immune stimulation in the colon
Evidence from Studies
Supporting (1)
Community contributions welcome
The improved effect and its mechanism of phytic acid on DSS-induced UC mice.
Contradicting (0)
Community contributions welcome
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