Rebamipide inhibited expression of TLR4 and TNF-alpha release in pulmonary epithelial cell line A549 induced by lipopolysaccharide.
- Author:
Xiufang WEN
1
;
Xia CHEN
;
Xiangdong ZHOU
Author Information
1. Department of Respiratory Medicine, Third People's Hospital of Chongqing, Chongqing 400014, China wenranran221@126.com
- Publication Type:Journal Article
- MeSH:
Alanine;
analogs & derivatives;
pharmacology;
Anti-Inflammatory Agents, Non-Steroidal;
pharmacology;
Cell Line;
Epithelial Cells;
cytology;
Humans;
Lipopolysaccharides;
pharmacology;
Lung;
cytology;
metabolism;
Quinolones;
pharmacology;
Toll-Like Receptor 4;
genetics;
metabolism;
Tumor Necrosis Factor-alpha;
genetics;
metabolism
- From:
Journal of Central South University(Medical Sciences)
2009;34(5):457-160
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To determine the effect of rebamipide on the expression of Toll-like recepter 4 (TLR4) and TNF-alpha release in pulmonary epithelial cell line A549.
METHODS:Lipopolysaccharide (LPS) was used to induce A549 in vitro, which was divided into 4 groups: a control group, a model group(LPS), and 2 intervention groups (10 mg/L rebamipide plus LPS; 30 mg/L rebamipide plus LPS). TNF-alpha release was detected with ELISA and expression of TLR4 was detected with RT-PCR and Western blot.
RESULTS:A549 cells were stimulated with LPS and TNF-alpha release was increased compared with the control group (P<0.01), peaking at 6 h. Expression of TLR4 was also increased compared with the control group (P<0.01), but it was inhibited by rebamipide compared with the model group (P<0.05). There was no significant difference between the 2 intervention groups (P>0.05).
CONCLUSION:The antiinflammatory mechanism of rebamipide may be reducing cytokine release by inhibiting TLR4 expression. Rebamipide may be used as a supplementary anti-infection drug.
