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Inhibition of c-Jun NH2-terminal kinase or extracellular signal-regulated kinase improves lung injury
- Title
- Inhibition of c-Jun NH2-terminal kinase or extracellular signal-regulated kinase improves lung injury
- Authors
- Lee H.S.; Kim H.J.; Moon C.S.; Chong Y.H.; Kang J.L.
- Ewha Authors
- 이지희; 정영해
- SCOPUS Author ID
- 이지희; 정영해
- Issue Date
- 2004
- Journal Title
- Respiratory Research
- ISSN
- 1465-993X
- Citation
- Respiratory Research vol. 5
- Indexed
- SCIE; SCOPUS
- Document Type
- Article
- Abstract
- Background: Although in vitro studies have determined that the activation of mitogen-activated protein (MAP) kinases is crucial to the activation of transcription factors and regulation of the production of proinflammatory mediators, the roles of c-Jun NH2-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) in acute lung injury have not been elucidated. Methods: Saline or lipopolysaccharide (LPS, 6 mg/kg of body weight) was administered intratracheally with a 1-hour pretreatment with SP600125 (a JNK inhibitor; 30 mg/kg, IO), or PD98059 (an MEK/ERK inhibitor; 30 mg/kg, IO). Rats were sacrificed 4 hours after LPS treatment. Results: SP600125 or PD98059 inhibited LPS-induced phosphorylation of JNK and ERK, total protein and LDH activity in BAL fluid, and neutrophil influx into the lungs. In addition, these MAP kinase inhibitors substantially reduced LPS-induced production of inflammatory mediators, such as CINC, MMP-9, and nitric oxide. Inhibition of JNK correlated with suppression of NF-κB activation through downregulation of phosphorylation and degradation of IκB-α, while ERK inhibition only slightly influenced the NF-κB pathway. Conclusion: JNK and ERK play pivotal roles in LPS-induced acute lung injury. Therefore, inhibition of JNK or ERK activity has potential as an effective therapeutic strategy in interventions of inflammatory cascade-associated lung injury. © 2004 Lee et al; licensee BioMed Central Ltd.
- DOI
- 10.1186/1465-9921-5-23
- Appears in Collections:
- 의과대학 > 의학과 > Journal papers
- Files in This Item:
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