2007International Journal of NeuroscienceRequires access

YULDA-HANSO-TANG ATTENUATES THE ENDOTOXIN-INDUCED INFLAMMATORY CYTOKINE PRODUCTION IN PERIPHERAL BLOOD MONONUCLEAR CELLS

Hyun‐Ja Jeong, Sujin Kim, Hyung‐Min Kim, Jae‐Young Um, Phil‐Dong Moon, Sug-Min Jun, Seung‐Heon Hong

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Abstract

Yulda-Hanso-Tang (YHT) has been used as a formula for the cerebral infarction (CI) patients. This study investigated the anti-inflammatory effects and possible mechanism of YHT on lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells. The amount of interleukin-1beta, IL-4, IL-6, IL-8, and tumor necrosis factor-alpha was increased in the LPS-treated cells. But, increased cytokine was inhibited by YHT except IL-8. The study showed that YHT inhibited the IL-1beta mRNA expression. YHT also inhibited LPS-induced activation of NF-kappaB and degradation of IkappaBalpha. These results suggest that YHT is an inhibitor of NF-kappaB, which might explain its beneficial effect in the treatment of inflammatory diseases.

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What this paper is about

Yulda-Hanso-Tang (YHT) has been used as a formula for the cerebral infarction (CI) patients. This study investigated the anti-inflammatory effects and possible mechanism of YHT on lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells. The amount of interleukin-1beta, IL-4, IL-6, IL-8, and tumor necrosis factor-alpha was increased in the LPS-treated cells. But, increased cytokine was inhibited by YHT except IL-8. The study showed that YHT inhibited the IL-1beta mRNA expression. YHT also inhibited LPS-induced activation of NF-kappaB and degradation of IkappaBalpha. These results suggest that YHT is an inhibitor of NF-kappaB, which might explain its beneficial effect in the treatment of inflammatory diseases.

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Available abstract

Yulda-Hanso-Tang (YHT) has been used as a formula for the cerebral infarction (CI) patients. This study investigated the anti-inflammatory effects and possible mechanism of YHT on lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells. The amount of interleukin-1beta, IL-4, IL-6, IL-8, and tumor necrosis factor-alpha was increased in the LPS-treated cells. But, increased cytokine was inhibited by YHT except IL-8. The study showed that YHT inhibited the IL-1beta mRNA expression. YHT also inhibited LPS-induced activation of NF-kappaB and degradation of IkappaBalpha. These results suggest that YHT is an inhibitor of NF-kappaB, which might explain its beneficial effect in the treatment of inflammatory diseases.

Key concepts: Peripheral blood mononuclear cell, Lipopolysaccharide, Cytokine, Tumor necrosis factor alpha, Interleukin 6, Interleukin, Inflammation, Immunology

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