Inhibitory effect of Cortex mori on the substance P-induced mast cell degranulation, granular leukocyte infiltraion, and vascular permeability in vivo

Chai, Ok Hee; Jung, Sung Ho; Lee, Moo Sam

Abstract

Cortex mori (Morus alba L.), the root bark of mulberry tree, has been used as an antiphlogistic, diuretic, and expectorant in herbal medicine. It has been reported tha hot water extract of Cortex mori has an inhibitory effect on substance P- and compound 48/80-induced mast cell degranulation and histamine release from rat peritoneal mast cells. Substance P (SP), a decapeptide which is present in sensory neurons, is believed to be a major mediator of neurogenic inflammations. N-terminal peptide of SP causes mast cell degranulation and its C-terminal peptide directly activates vascular endothelial cells to increase the vascular permeability. It has recently been shown that SP induces leukocyte infiltration in the skin, which is mediated through mast cell degranulation. The purpose of this study was to investigate whether Cortex mori could inhibit SP-induced leukocyte infiltration in mouse skin. Subcutaneous administration of SP (10(-8) to 10(-5) M) induced leukocytes infiltration in the skin of BALB/c mice 8h after the injection. Leukocyte infiltration of mouse skin was associated with mast cell degranulation which was induced by SP1-9 (10(-7) to 10(-5) M), but not by SP6-11 (10(-7) to 10(-5) M) which was found to increase the vascular permeability of endothelial cells in mouse skin. However, SP6-11 (10(-7) to 10(-5) M) enhanced SP1-9-induced leukocyte infiltration in the skin without any significant increase in mast cell degranulation. Cortex mori (10 mg/ml) inhibited SP- and SP1-9-induced mast cell degranulation, but did not inhibite SP6-11-induced increase in vascular perameability. Taken together, the data indicate that the hot water extract of Cortex mori contains some substances with an activity to inhibit SP-induced leukocyte infiltration in to the mous skin. These activity of Cortex mori is likely due to the inhibition of release of chemical mediators from the mast cells which participate in neurogenic inflammations.