Tetrandrine suppresses pro-inflammatory mediators in PMA plus A23187-induced HMC-1 cells

Tetrandrine (TET), a bis-benzylisoquinoline alkaloid from the root of Stephania tetrandra, is known to possess antitumor activity in various malignant neoplasms. However, the precise mechanism of TET-mediated immune modulation remains to be clarified. One of the possible mechanisms for its protectiv...

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Published in:International journal of molecular medicine 2014-05, Vol.33 (5), p.1335-1340
Main Authors: KANG, OK-HWA, AN, HYEON-JIN, KIM, SUNG-BAE, MUN, SU-HYUN, SEO, YUN-SOO, JOUNG, DAE-KI, CHOI, JANG-GI, SHIN, DONG-WON, KWON, DONG-YEUL
Format: Article
Language:English
Subjects:
Alkaloids
Binding sites
Care and treatment
Cytokines
Gene expression
Health aspects
human mast cell
Immune response
Immunoglobulins
Inflammation
Kinases
Observations
Phosphorylation
pro-inflammatory mediator
Proteins
Regulation
Studies
tetrandrin
Tumor necrosis factor-TNF
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Summary:Tetrandrine (TET), a bis-benzylisoquinoline alkaloid from the root of Stephania tetrandra, is known to possess antitumor activity in various malignant neoplasms. However, the precise mechanism of TET-mediated immune modulation remains to be clarified. One of the possible mechanisms for its protective properties is by downregulation of the inflammatory responses. In the present study, the human mast cell line (HMC-1) was used to investigate this effect. TET significantly inhibited the induction of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-8 by phorbol 12-myristate 13-acetate (PMA) plus A23187. Moreover, TET attenuated expression of cyclooxygenase (COX)-2. In activated HMC-1 cells, the phosphorylation of extra-signal response kinase (ERK1/2) and c-jun N-terminal Kinase (JNK1/2), but not p38 mitogen-activated protein kinase, was decreased by treatment of the cells with TET. TET inhibited PMA plus A23187-induced nuclear factor (NF)-κB activation, IκB degradation and phosphorylation. Furthermore, TET suppressed the expression of TNF-α, IL-8, IL-6 and COX-2 through suppression of the ERK1/2, JNK1/2, IκBα degradation and phosphorylation, and NF-κB activation. These results indicated that TET exerted a regulatory effect on inflammatory reactions mediated by mast cells.
ISSN:1107-3756
1791-244X
DOI:10.3892/ijmm.2014.1683