Objective: To explore anti-inflammation and mechanism of Qinghuachang Decoction (QD) by using LPS stimulated differentiated colon cancer Caco-2 cells (as an inflammation model of human enterocytes).
Methods: QD was prepared. Human colonic epithelial Caco-2 cells were cultured. Expressions of TNF-alpha and IL-8 were determined using ELISA. Expressions of inhibitory Kaba protein (IkappaB-alpha), phosphorylated inhibitory Kaba protein (p-lkappaB-alpha), nuclear transcription factor p50 (p50), and nuclear transcription factor ReIA (ReIA) protein were determined by Western blot.
Results: Compared with the negative control group (without LPS stimulation), LPS stimulated the release of IL-8 and TNF-alpha in Caco-2 cells (P < 0.05). QD treatment could reduce the secretion of TNF-alpha and IL-8 induced by LPS in a dose dependent manner (P < 0.05). QD at 0, 5, 10, and 50 microg/mL had no significant effect on Caco-2 cell survival rates (P > 0.05), with no statistical difference among various concentrations (P > 0.05). QD could significantly suppress nuclear factor-kappa B (NF-kappaB) phosphorylation stimulated by LPS. The expression of p-IKappaB-alpha was decreased with increasing concentrations of QD (P < 0.05). There was no obvious change in IKB-alphaB expressions (P > 0.05). Expressions of p50 and ReIA decreased with increasing concentrations of QD (P < 0.05). Both of them were in a dose dependent manner.
Conclusion: QD inhibited LPS mediated NF-kappaB activation, which might be one of its mechanisms for treating inflammatory bowel disease (IBD).
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