Korean J Physiol Pharmacol.  1997 Aug;1(4):445-456.

Effects of ginsenosides on the mechanism of histamine release in the guinea pig lung mast cells activated by specific antigen-antibody reactions

  • 1Department of Pharmacology, Yonsei University, College of Medicine, CPO Box 8044, Seoul 120-752, South Korea.


We previously reported that some components of ginsenosides decreased mediator releases evoked by the activation of mast cells with specific antigen-antibody reactions. This study aimed to assess the effects of ginsenosides (Rb2, Re) on the mechanism of histamine release in the mast cell activation. We partially purified guinea pig lung mast cells by using enzyme digestion, the rough and the discontinuous percoll density gradient method. Mast cells were sensitized with IgG1 and challenged with ovalbumin (OA). Histamine was assayed by fluorometric analyzer, leukotrienes by radioimmunoassay. Phospholipase D (PLD) activity was assessed more directly by the production of (3H)phosphatidylbutanol (PBut) which was produced by PLD-mediated transphosphatidylation in the presence of butanol. The amount of 1,2-diacylglycerol (DAG) were measured by the (3H)DAG labeled with (3H)palmitic acid or (3H)myristic acid. Pretreatment of Rb2 (300 microgram) significantly decreased histamine release by 60%, but Re (300 gg) increased histamine release by 34%. Leukotrienes release in Rb2 was decreased by 40%, Re was not affected in the leukotrienes release during mast cell activations. An increasing PLD activity during mast cell activation was decreased by the dose-dependent manner in the pretreatment of Rb2, but Re pretreatment facilitated the increased PLD activity during mast cell activation. The amount of DAG produced by phospholipase C (PLC) activity was decreased by Rb2 pretreatment, but Re pretreatment was not affected. The amount of mass DAG was decreased by Rb2 and Re pretreatment during mast cell activation. The data suggest that Rb2 purified from Korean Red Ginseng Radix inhibits the DAG which is produced by the activation of mast cells with antigen-antibody reactions via both phosphatidylinositide-PLC and phosphatidylcholine-PLD systems, and then followed by the inhibition of histamine release. However, Re increases histamine release by stimulation of DAG production, which is mediated by phosphatidylcholine-PLD system rather than by phosphatidylinositide-PLC system, but inhibits the mass DAG production. Thus, it could be inferred that other mechanisms play a role in the increase of histamine release during mast cell activation.


Mast cell; Histamine; Leukotrienes; Phospholipase D; Phospholipase C; 1,2-diacylglycerol; Phosphatidylbutanol
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