Nutrition Research and Practice

The Korean Nutrition Society (한국영양학회)
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A standardized bamboo leaf extract inhibits monocyte adhesion to endothelial cells by modulating vascular cell adhesion protein-1

  • Choi, Sunga (Infectious Signaling Network Research Center and Research Institute for Medical Sciences, Department of Physiology, School of Medicine, Chungnam National University) ;
  • Park, Myoung Soo (Infectious Signaling Network Research Center and Research Institute for Medical Sciences, Department of Physiology, School of Medicine, Chungnam National University) ;
  • Lee, Yu Ran (Infectious Signaling Network Research Center and Research Institute for Medical Sciences, Department of Physiology, School of Medicine, Chungnam National University) ;
  • Lee, Young Chul (Unigen Inc.) ;
  • Kim, Tae Woo (Unigen Inc.) ;
  • Do, Seon-Gil (Life Science Research Institute, Univera Inc.) ;
  • Kim, Dong Seon (Unigen Inc.) ;
  • Jeon, Byeong Hwa (Infectious Signaling Network Research Center and Research Institute for Medical Sciences, Department of Physiology, School of Medicine, Chungnam National University)
  • Received : 2012.09.04
  • Accepted : 2012.12.07
  • Published : 2013.02.01
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Abstract

Bamboo leaves (Phyllostachys pubescens Mazel ex J. Houz (Poacea)) have a long history of food and medical applications in Asia, including Japan and Korea. They have been used as a traditional medicine for centuries. We investigated the mechanism of anti-inflammatory activity of a bamboo leaf extract (BLE) on tumor necrosis factor-alpha (TNF-${\alpha}$)-induced monocyte adhesion in human umbilical vein endothelial cells (HUVECs). Exposure of HUVECs to BLE did not inhibit cell viability or cause morphological changes at concentrations ranging from 1 ${\mu}g/ml$ to 1 mg/ml. Treatment with 0.1 mg/ml BLE caused 63% inhibition of monocyte adhesion in TNF-${\alpha}$-activated HUVECs, which was associated with 38.4% suppression of vascular cell adhesion molecule-1 expression. Furthermore, TNF-${\alpha}$-induced reactive oxygen species generation was decreased to 47.9% in BLE treated TNF-${\alpha}$-activated HUVECs. BLE (0.05 mg/ml) also caused about 50% inhibition of interleukin-6 secretion from lipopolysaccharide-stimulated monocyte. The results indicate that BLE may be clinically useful as an anti-inflammatory or anti-oxidant for human cardiovascular disease including atherosclerosis.

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References

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