Abstract:
:This study was performed to evaluate the effects of epigallocatechin 3 gallate (EGCG) on lipopolysaccharide (LPS)-induced acute lung injury in a murine model. In the present study, production of TNF-alpha and MIP-2 and activation of extracellular signal-regulated kinases (ERK)1/2, c-Jun amino terminal kinases (JNK) and p38 in RAW264.7 cells were measured. EGCG inhibited the production of TNF-alpha and MIP-2, and attenuated phosphorylation levels of ERK1/2 and JNK, but not p38 in RAW264.7 cells stimulated with LPS. Also, EGCG attenuated the production of TNF-alpha and MIP-2, and the phosphorylation of ERK1/2 and JNK in the lungs of mice administered with LPS intratracheally. It reduced wet/dry weight ratio, histological severities, and neutrophil accumulation in the lungs in mice given LPS. Our results showed that EGCG attenuated LPS-induced lung injury by suppression of the MIP-2 and TNF-alpha production, and ERK1/2 and JNK activation in macrophage stimulated with LPS.
journal_name
Inflammationjournal_title
Inflammationauthors
Bae HB,Li M,Kim JP,Kim SJ,Jeong CW,Lee HG,Kim WM,Kim HS,Kwak SHdoi
10.1007/s10753-009-9161-zsubject
Has Abstractpub_date
2010-04-01 00:00:00pages
82-91issue
2eissn
0360-3997issn
1573-2576journal_volume
33pub_type
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