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KMID : 0360419940300020243
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Korean Journal of Pharmacology
1994 Volume.30 No. 2 p.243 ~ p.254
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The Effects of Single Component of Ginsenosides on the Mechanism of Mediator Release in the Allergic Hypersensitivity
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Abstract
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Inflammatory diseases, allergic and asthmatic disorders are caused by the mediator release from the activation of the phospholipase C (PLC), phospholipase D (PLD), methyltransf erase or adenylate cyclase etc, during IgG or IgE cross-linking of high affinity receptors on mast cells or basophil surface. One important enzyme activated after IgG or IgE receptor cross-linking is PLD, the enzyme which converts phosph´3tidylcholine (PC) to phosphatidic acid (PA). Under the hypothesis that these may be some d fferences in mediator release according to the difference in PLD activity, we attempted to confirm the ginseng saponin effects on the PLD activity. We ex-
amined the PLD activity during the passively sensitized mast cell activation in the presence of single component of ginsenosides (Rc, Rgi, RgZ, Rg3). We also measured the amount of media-
tors (histamine and leukotrienes) released by stimulating with ovalbumin (OA) or calcium ionophore (Cal), Guinea Pig lung´-mast cells were purified using enzyme digestion, count current elutriation, and discontinuous Percoll density gradient, In purified mast cellsprelabeled with [3I-1] arachidonic acid or [´H] palmitic acid, PLD activity was assessed more directly by the production of labeled PEt by PLD-mediated transphosphatidylation in the presence of ethanol. H istanine release was determined by Spectrophotofluorometry, and leukotrienes by radioimmunoassay.
The PLD activity during the passively sensitized mast cell activation is increased up to 3-V 5times. The PLD activity during the passively sensitized mast cell activation in the presence of all ginsenosides is decreased up to 4?11 times. Rg, and Rg2 ginsenoside pretreatment decreased histamine and leukotrienes by 50% in the OA-induced or by 40% in the Cal-induced mast cell after passively sensitization. Rc pretreatment poorly decreased histamine but leukotrienes de-creased by 70% in the OA-induced or by 35% in the Cal-induced mast cell. Rg3 ginsenoside pre-treatment increased histamine release without challenging OA or Cal but leukotrienes decreased.
These observations indicate that single unit of ginsenosides may be an important contributor to inhibit the release of histamine and leukotrienes in the guinea pig lung mast cells, that inhibits the PLD-mediated formation of DAG evoked by mast cell activation.
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