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J.Health Sci., 54(4), 416-422, 2008
Mosla dianthera Decreases Immediate-Type Allergic Reaction and Tumor Necrosis Factor-α Production
Sang-Hyun Kim,a, # Hoon Jeon,b, #
Soyoung Lee,a Hee-Young Son,a
Seung-Bin Park,a Mi-Sun Kim,a
Eun-Ju Choi,a Jong-Pil Lim,b
Jae-Soon Eun,b Jeong-Suk Park,c
and Tae-Yong Shinb, *
aCell & Matrix Research Institute, Department of Pharmacology, School of Medicine, Kyungpook National University , 101 Dongindong 2 Ga, Jung-gu, Daegu 700-422, Republic of Korea,
bCollege of Pharmacy, Woosuk University, 490 Hujeong-ri, Samrye-eup, Wanju-gun, Jeonbuk 565-701, Republic of Korea and
cDepartment of Oriental AlternativeMedicine, Nambu University, 864-1 Wolgyedong, Gwangsan-gu, Gwangju 506-706, Republic of Korea
Immediate-type hypersensitivity is involved in many allergic diseases such as asthma, allergic rhinitis, and sinusitis. The discovery of drugs for the treatment of allergic disease is an important subject in human health. Stimulation of mast cells releases inflammatory mediators, such as histamine, and proinflammatory cytokines with immune regulatory properties. We investigated the effect of the aqueous extract of Mosla dianthera (M. dianthera) (Maxim) (AEMD) on the immediate-type allergic reaction and studied its possible mechanisms of action using the model of mast cell-mediated allergic reaction. AEMD dose dependently inhibited compound 48/80-induced systemic allergic reaction and serum histamine release in mice. AEMD attenuated immunoglobulin E (IgE)-mediated skin allergic reaction and histamine release from mast cells. In addition, AEMD decreased the gene expression and production of tumor necrosis factor (TNF)-α in phorbol 12-myristate 13-acetate (PMA) and calcium ionophore A23187-stimulated human mast cells. Our findings provide evidence that AEMD inhibits the mast cell-derived allergic reaction and that TNF-α is involved in these effects. These findings indicate that AEMD could be a candidate as an antiallergic agent.
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