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Biomed Rep. 2014 Jan;2(1):63-68. Epub 2013 Oct 3.

In vitro effects of emodin on peritoneal macrophage intercellular adhesion molecule-3 in a rat model of severe acute pancreatitis/systemic inflammatory response syndrome.

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  • 1Department of General Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, P.R. China.
  • 2Department of Pharmacy, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, P.R. China.

Abstract

Rhubarb is often used in Chinese herbal medicine for the treatment of systemic inflammatory response syndrome (SIRS). Emodin is the main active constituent of rhubarb. This study was performed to investigate the in vitro effects of emodin and dexamethasone on peritoneal macrophage (pMΦ) phagocytosis and the expression of intercellular adhesion molecule-3 (ICAM-3). A total of 40 Sprague-Dawley (SD) rats were randomly divided into sham surgery (n=10) and model groups (n=30). After 24 h, pMΦs were harvested and the model group was randomly divided into three subgroups (n=10 rats/subgroup): the 5 μg/ml emodin, 0.1 μmol/ml dexamethasone and control groups. The drugs were administered following macrophage (MΦ) adhesion for 24 h. pMΦ phagocytosis was significantly increased in the emodin group compared to that in the control group. Moreover, pMΦ phagocytosis was significantly increased in the emodin group compared to that in the dexamethasone group. The expression of ICAM-3 was significantly increased in the emodin group compared to that in the control group. The expression of ICAM-3 was significantly increased in the emodin group compared to that in the dexamethasone group. The expression of ICAM-3 was significantly increased in the emodin and dexamethasone groups compared to that in the control group. pMΦ phagocytosis and ICAM-3 expression were significantly increased following emodin treatment compared to those in the control and dexamethasone groups, indicating that emodin may enhance pMΦ phagocytosis and apoptotic cell clearance by altering ICAM-3 expression.

KEYWORDS:

emodin; intercellular adhesion molecule-3; macrophage; severe acute pancreatitis

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