The novel role of platelet-activating factor in protecting mice against lipopolysaccharide-induced endotoxic shockopen access
- Authors
- Jeong, Young-Il; Jung, In Duk; Lee, Chang-Min; Chang, Jeong Hyun; Chun, Sung Hak; Noh, Kyung Tae; Jeong, Soo kyung; Shin, Yong Kyoo; Lee, Won Suk; Kang, Mi Sun; Lee, Sang-Yull; Lee, Jae-Dong; Park, Yeong-Min
- Issue Date
- Aug-2009
- Publisher
- Public Library of Science
- Citation
- PLoS ONE, v.4, no.8
- Journal Title
- PLoS ONE
- Volume
- 4
- Number
- 8
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/23429
- DOI
- 10.1371/journal.pone.0006503
- ISSN
- 1932-6203
- Abstract
- Background: Platelet-activating factor (PAF) has been long believed to be associated with many pathophysiological processes during septic shock. Here we present novel activities for PAF in protecting mice against LPS-mediated endotoxic shock. Principal Findings: In vivo PAF treatment immediately after LPS challenge markedly improved the survival rate against mortality from endotoxic shock. Administration of PAF prominently attenuated LPS-induced organ injury, including profound hypotension, excessive polymorphonuclear neutrophil infiltration, and severe multiple organ failure. In addition, PAF treatment protects against LPS-induced lymphocytes apoptosis. These protective effects of PAF was correlated with significantly decreases in the production of the inflammatory mediators such as TNF-α, IL-1β, IL-12, and IFN-γ, while increasing production of the anti-inflammatory cytokine IL-10 in vivo and in vitro. Conclusions: Taken together, these results suggest that PAF may protect mice against endotoxic shock via a complex mechanism involving modulation of inflammatory and anti-inflammatory mediators. © 2009 Jeong et al.
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