Glucosamine regulation of LPS-mediated inflammation in human bronchial epithelial cells

Yuh Lin Wu*, Yu Ru Kou, Hui Ling Ou, Han Yun Chien, Kun Han Chuang, Han Hsun Liu, Tzong Shyuan Lee, Cheng Yen Tsai, Meng Lun Lu

*此作品的通信作者

研究成果: Article同行評審

24 引文 斯高帕斯(Scopus)

摘要

Inflammation is a complex process involving cytokine production to regulate host defense cascades in order to clear pathogenic agents. Upregulation of inflammatory cytokines, such as IL-6 and IL-8 by bacteria infection, occurs in pulmonary tissues and has been demonstrated to be critical to the lung inflammatory response. Glucosamine, primarily identified as an anti-arthritis supplement, has been also regarded as a potential anti-inflammatory agent. Thus we hypothesized that lipopolysaccharide (LPS) would activate IL-6 and IL-8 expressions in human primary bronchial epithelial cells and glucosamine could attenuate such an effect. The RT-PCR, real-time PCR, and ELISA analyses demonstrated that LPS-induced mRNAs encoding IL-6 and IL-8 and the subsequent secretion of IL-6 and IL-8 were inhibited by glucosamine treatment. MTT, alamarBlue, and annexin V apoptosis assays all suggested that this inhibition effect was not due to a cytotoxic effect mediated by glucosamine. Using the inhibitors of the MAP kinases and NFκB, it was revealed that p38, JNK and ERK, as well as NFκB, are all involved in LPS-induced IL-8 secretion; however only p38 is involved in LPS-induced IL-6 secretion. Immunoblot analysis further demonstrated that LPS-mediated phosphorylation of JNK and ERK, but not the LPS-induced NFκB translocation, was inhibited by glucosamine. Altogether, our results indicate that glucosamine can potently suppress LPS-induced inflammatory cytokine expression, at least in part via attenuation of MAPK activation.

原文English
頁(從 - 到)219-226
頁數8
期刊European Journal of Pharmacology
635
發行號1-3
DOIs
出版狀態Published - 6月 2010

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