Paeoniflorin Prevents Intestinal Barrier Disruption and Inhibits Lipopolysaccharide (LPS)-Induced Inflammation in Caco-2 Cell Monolayers

• Published in: Inflammation Vol. 42; no. 6; pp. 2215 - 2225
• Main Authors: Wu, Xi-Xi, Huang, Xie-Lin, Chen, Ru-Ru, Li, Tang, Ye, Hua-Jun, Xie, Wei, Huang, Zhi-Ming, Cao, Gao-Zhong
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.12.2019; Springer Nature B.V
• Subjects: Anti-Inflammatory Agents - pharmacology; Bioactive compounds; Biomedical and Life Sciences; Biomedicine; Caco-2 Cells; Cyclooxygenase-2; Dextran; Epithelium; Gelatinase B; Glucosides - pharmacology; Glucosides - therapeutic use; Humans; Immunology; Inflammation - chemically induced; Inflammation - prevention & control; Inflammatory bowel disease; Inflammatory bowel diseases; Interleukin 6; Internal Medicine; Intestinal Mucosa - drug effects; Intestine; Intestines - drug effects; Intestines - pathology; Lipopolysaccharides; Matrix metalloproteinase; Metalloproteinase; Monoterpenes - pharmacology; Monoterpenes - therapeutic use; NF-κB protein; Nitric oxide; Nitric-oxide synthase; Original Article; Pathology; Permeability; Permeability - drug effects; Pharmacology/Toxicology; Rheumatology; Tumor necrosis factor-TNF; Tumor necrosis factor-α; Unilamellar Liposomes; Zonula occludens-1 protein; NF-κB; intestinal barrier; tight junction protein; Nrf2/OH-1; paeoniflorin
• ISSN: 0360-3997; 1573-2576; 1573-2576
• DOI: 10.1007/s10753-019-01085-z

Inflammatory bowel disease (IBD) in humans is closely related to bacterial infection and the disruption of the intestinal barrier. Paeoniflorin (PF), a bioactive compound from Paeonia lactiflora Pallas plants, exerts a potential effect of anti-inflammatory reported in various researches. However, the effect of PF on intestinal barrier function and its related mechanisms has not been identified. Here, we investigate the PF potential anti-inflammatory effect on lipopolysaccharide (LPS)-stimulated human Caco-2 cell monolayers and explore its underlying key molecular mechanism. In this context, PF significantly increased TEER value, decreased intestinal epithelium FITC-dextran flux permeability, and restored the expressions of occludin, ZO-1, and claudin5 in LPS-induced Caco-2 cell. In vitro , treatment of PF significantly inhibited LPS-induced expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), and matrix metalloproteinase-9 (MMP-9). In addition, we found that PF suppressed nuclear factor kappa B (NF-κB) signaling via activating the Nrf2/HO-1 signaling pathways in ILPS-stimulated Caco-2 cells. Our findings indicate that PF has an inhibitory effect on endothelial injury. Our findings suggested that PF has an anti-inflammatory effect in ILPS-stimulated Caco-2 cells, which might be a potential therapeutic agent against IBD and intestinal inflammation.