Anti‑inflammatory effects of oridonin on an in vitro model using LPS‑treated human intestinal Caco‑2 cells

Oridonin (Ori) attenuates dextran sulfate sodium‑induced ulcerative colitis (UC) in mice, and its underlying mechanism involves the sirtuin 1 (SIRT1)/NF‑κB/p53 pathway. In the present study, lipopolysaccharide (LPS)‑stimulated Caco‑2 cells were used as an in vitro model to mimic human intestinal epithelial inflammation, to ascertain the anti‑inflammatory effects of Ori on a cell model of UC. The concentrations of TNF‑α and IL‑1β were quantified using ELISA, the expression levels of SIRT1, NF‑κB and p53 were assessed through western blot analysis, and cell viability was determined using the Cell Counting Kit‑8. The results showed that cell viability was affected by treatment with Ori at different doses. Ori significantly inhibited the optical density values in a dose‑dependent manner at the doses of 5.0‑80.0 µM whereas it did not affect viability at the doses of 0.625‑2.50 µM, compared with in the control group. These findings suggested that the inhibitory effect of Ori on intestinal epithelial cells did not result from cytotoxic action at the doses of 0.625‑2.50 µM. Furthermore, Ori suppressed the inflammatory response in intestinal epithelial cells by significantly reducing LPS‑induced secretion of the pro‑inflammatory cytokines TNF‑α and IL‑1β with a ~2‑fold reduction. Additionally, Ori significantly increased the protein expression levels of SIRT1, and decreased the protein expression levels of NF‑κB and p53. In conclusion, the present results indicated that the inhibition of NF‑κB‑mediated inflammation may be a key mechanism by which Ori exerts its therapeutic effects on UC.