Ephedrine hydrochloride inhibits PGN-induced inflammatory responses by promoting IL-10 production and decreasing proinflammatory cytokine secretion via the PI3K/Akt/GSK3β pathway View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-07

AUTHORS

Yuejuan Zheng, Yang Yang, Yuhu Li, Limin Xu, Yi Wang, Ziyi Guo, Haiyan Song, Muyi Yang, Beier Luo, Aoxiang Zheng, Ping Li, Yan Zhang, Guang Ji, Yizhi Yu

ABSTRACT

Approaches for controlling inflammatory responses and reducing the mortality rate of septic patients remain clinically ineffective; new drugs need to be identified that can induce anti-inflammatory responses. Ephedrine hydrochloride (EH) is a compound that is widely used in cardiovascular diseases, especially to treat hypotension caused by either anesthesia or overdose of antihypertensive drugs. In this study, we reported that EH also plays an important role in the control of the inflammatory response. EH increased IL-10 and decreased proinflammatory cytokine (IL-6, tumor-necrosis factor (TNF)-α, IL-12 and IL-1β) expression in primary peritoneal macrophages and Raw264.7 cells treated with peptidoglycan (PGN), a Gram-positive cell wall component. The anti-inflammatory role of EH was also demonstrated in an experimental mouse model of peritonitis induced by intraperitoneal PGN injection. The phosphatidylinositol 3-kinase (PI3K)/Akt pathway was found to be responsible for the EH-mediated increase in IL-10 production and decrease in IL-6 expression. Therefore, our results illustrated that EH can help maintain immune equilibrium and diminish host damage by balancing the production of pro- and anti-inflammatory cytokines after PGN challenge. EH may be a new potential anti-inflammatory drug that can be useful for treating severe invasive Gram-positive bacterial infection. More... »

PAGES

cmi20133

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/cmi.2013.3

DOI

http://dx.doi.org/10.1038/cmi.2013.3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1016925979

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/23604046


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