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학술저널
저자정보
Choi, In-Young (Department of Pharmacology, College of Oriental Medicine, Institute of Oriental Medicine, Kyung Hee University) Na, Ho-Jeong (Department of Pharmacology, College of Oriental Medicine, Institute of Oriental Medicine, Kyung Hee University) Um, Jae-Young (Department of Pharmacology, College of Oriental Medicine, Institute of Oriental Medicine, Kyung Hee University) Kim, Hyung-Min (Department of Pharmacology, College of Oriental Medicine, Institute of Oriental Medicine, Kyung Hee University) Hong, Seung-Heon (College of Pharmacy, Wonkwang University) Sim, Kuk-Jin (College of Oriental Medicine, Wonkwang University) Song, Bong-Keun (College of Oriental Medicine, Wonkwang University) Nam, Gi-Hye (Department of Hygienic Chemistry, College of Pharmacy, Kyung Hee University) Choung, Se-Young (Department of Hygienic Chemistry, College of Pharmacy, Kyung Hee University) Jeong, Hyun-Ja (Biochip Research Center, Hoseo University)
저널정보
경희한의학연구센터 Oriental pharmacy and experimental medicine Oriental pharmacy and experimental medicine 제10권 제1호
발행연도
2010.1
수록면
7 - 12 (6page)

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Typha orientalis' stem (TOS) is traditionally used as an herbal medicine for difficulty in urination, galactophoritis purulenta, whooping cough, and allergic dermatitis. However, its effect in experimental models remains unknown. Here, we report the effect of TOS on the phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187-induced inflammatory cytokine production and extracellular signal-regulated kinase (ERK) activation in the human mast cell line, HMC-1. TOS inhibited PMA plus A23187-induced cytokines such as tumor necrosis factor-alpha (TNF-$\alpha$) and interleukin (IL)-6. Maximal inhibition rate of TNF-$\alpha$ and IL-6 production by TOS (1 mg/ml) was about 44.02%, and 45.20%, respectively (P < 0.05). In addition, TOS inhibited the expression of TNF-$\alpha$ and IL-6 mRNA under the same condition. Moreover, TOS partially blocked PMA plus A23187-induced ERK phosphorylation. These results suggested TOS could inhibit the cytokine production through blocking of ERK activity.

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