Resveratrol attenuates intestinal epithelial barrier dysfunction via Nrf2/HO-1 pathway in dextran sulfate sodium-induced Caco-2 cells.
Level 5 - mechanism / opinion, no new human data
In vitro bench research and network pharmacology study with no human data
PubMed 38372468 · doi:10.1002/iid3.1193
What was done
Researchers evaluated the protective effects of resveratrol against dextran sulfate sodium (DSS)-induced barrier damage in Caco-2 intestinal epithelial cells. Inflammatory cytokines (IL-6, IL-1β, TNF-α, IL-10) were quantified using ELISA, and monolayer integrity was evaluated via transepithelial electrical resistance (TEER). Tight junction protein expression (ZO-1 and Occludin) was assessed by immunofluorescence and Western blot. Network pharmacology identified putative pathways, and Nrf2 and HO-1 protein levels were analyzed by Western blot.
What was found
The abstract reports directional changes without numeric values or confidence intervals. Resveratrol increased cell viability and IL-10 concentrations while reducing TNF-α, IL-6, and IL-1β levels. Resveratrol increased TEER values, upregulated ZO-1 and Occludin tight junction protein expression, and augmented Nrf2 and HO-1 protein expression.
Why it matters
The study outlines a cellular mechanism by which resveratrol preserves intestinal epithelial tight junction integrity and reduces inflammatory signaling via the Nrf2/HO-1 pathway in an in vitro model of colitis.
Limits
The study is restricted to an in vitro immortalized cell line (Caco-2) and in silico network pharmacology; no in vivo animal or human data were generated. The abstract presents no numerical data, concentrations, effect sizes, or measures of variance. Resveratrol's low human oral bioavailability was not addressed.
Cited by
- supports NRF2 induction promotes the sealing of tight junctions in enterocytes, reducing endotoxin translocation and inflammation.