• Hong-Beom Bae, Mei Li, Jong-Phil Kim, Seok-Jai Kim, Cheol-Won Jeong, Hyung-Gon Lee, Woong-Mo Kim, Hyung-Seok Kim, and Sang-Hyun Kwak.
• Department of Anesthesiology and Pain Medicine, Chonnam National University, Medical School, 5 Hak dong, Gwangju, 501 746, South Korea.
• Inflammation. 2010 Apr 1;33(2):82-91.

AbstractThis 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.

47 keywords...

hide…