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HMC05, Herbal Formula, Inhibits TNF-α-Induced Inflammatory Response in Human Umbilical Vein Endothelial Cells

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HINDAWI LTD
DOI: 10.1093/ecam/nep126

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  1. Ministry of Health & Welfare, Republic of Korea [B080031]
  2. Ministry of Commerce, Industry and Energy (MOCIE) [RTI04-01-04]
  3. Korea Health Promotion Institute [B080031] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Vascular inflammation has been implicated in the progression of cardiovascular diseases such as atherosclerosis. In the present study, we found that HMC05, an extract from eight different herbal mixtures, dose-dependently inhibited tumor necrosis factor-alpha (TNF-alpha)-induced adhesion of monocytes to endothelial cells. Such inhibitory effect of HMC05 correlated with suppressed expression of monocyte chemoattractant protein-1, CC chemokine receptor 2, vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1. In addition, HMC05 significantly inhibited production of reactive oxygen species (ROS) and nuclear factor (NF)-kappa B activation by TNF-alpha. Those inhibitory effects of HMC05 (1-10 mu g mL(-1)) on the TNF-alpha-induced inflammatory event was similar to those of berberine (1-10 mu M), which is a major component of HMC05 and one of herbal compounds known to have vasorelaxing and lipid-lowering activities. However, berberine significantly reduced the viability of HUVECs in a time-and concentration-dependent manner. In contrast, HMC05 (1-10 mu g ml(-1)) did not affect the cell viability for up to 48 h treatment. In conclusion, we propose that HMC05 may be a safe and potent herbal formula against vascular inflammation, and its action may be attributable to the inhibition of ROS- and NF-kappa B-dependent expression of adhesion molecules and chemokines.

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