Erschienen in:
01.04.2010
The Effect of Epigallocatechin Gallate on Lipopolysaccharide-Induced Acute Lung Injury in a Murine Model
verfasst von:
Hong-Beom Bae, Mei Li, Jong-Phil Kim, Seok-Jai Kim, Cheol-Won Jeong, Hyung-Gon Lee, Woong-Mo Kim, Hyung-Seok Kim, Sang-Hyun Kwak
Erschienen in:
Inflammation
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Ausgabe 2/2010
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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-α 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-α 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-α 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-α production, and ERK1/2 and JNK activation in macrophage stimulated with LPS.