Apigenin Alleviates Intestinal Ischemia/Reperfusion Injury via Upregulating Nrf2-Mediated Tight Junction Integrity.
Level 5 - mechanism / opinion, no new human data
Preclinical animal and in vitro cell culture study without human subjects.
PubMed 40150847 · doi:10.1002/mnfr.70043
What was done
Researchers evaluated the protective effects and mechanism of apigenin against intestinal ischemia/reperfusion (I/R) injury using in vivo and in vitro models. In vivo, 30 rats were randomly divided into five groups and subjected to superior mesenteric artery occlusion. In vitro, Caco-2 and IEC-6 epithelial cells were subjected to hypoxia and re-oxygenation (H/R). Markers of inflammation, oxidative stress, barrier integrity, and the Nrf2/HO-1 signaling pathway were assessed, including testing the effect of Nrf2 knockdown on tight junction protein expression.
What was found
Apigenin significantly reduced inflammatory cytokine release (TNF-α, IL-1β, IL-6, and MPO, p < 0.01), attenuated oxidative stress markers (MDA, SOD, GSH, and GSH-Px, p < 0.01), and improved barrier function markers (DAO and TEER, p < 0.01) in both rat and cell models compared to untreated I/R or H/R conditions, while having no significant effect in normal controls (p > 0.05). It also upregulated Nrf2, HO-1, and tight junction proteins (p < 0.01). Nrf2 knockdown abolished apigenin-induced tight junction upregulation. Exact quantitative measurements and effect sizes were not reported in the abstract.
Why it matters
This study delineates an Nrf2-dependent mechanism through which apigenin preserves epithelial tight junction integrity and dampens inflammation during gut ischemia/reperfusion, highlighting potential molecular targets for ischemic intestinal damage.
Limits
Findings are limited to rat and cell culture models, with no clinical validation in humans. The abstract omits apigenin dosages, treatment duration, and exact numerical values or effect sizes for the measured endpoints.
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