Ailanthus altissima swingle has anti-anaphylactic effect and inhibits inflammatory cytokine expression via suppression of nuclear factor-kappaB activation.
Ailanthus altissima swingle (ailanthic cortex, AAS) has been used as a traditional medicine for fever, bleeding, infection, and inflammation for many years in Korea. However, its mechanisms have not been examined. In the present study, we investigate the effect of AAS on the mast-cell-mediated allergic and inflammatory reaction using in vivo and in vitro models and elucidate its molecular mechanisms. AAS significantly inhibited compound 48/48-induced edema and systemic anaphylaxis. AAS significantly inhibited passive cutaneous anaphylaxis. AAS inhibited histamine release from rat peritoneal mast cells (RPMCs) in a dose-dependent manner. Moreover, AAS significantly inhibited production of inflammatory cytokines, tumor necrosis factor (TNF), interleukin (IL)-6, and IL-8 on the phorbol 12-myristate 13-acetate and calcium ionophore A23187 (PMACI)-stimulated human mast cell line, HMC-1 cells. AAS inhibits the IgE or stem cell factor-induced TNF production on RPMCs. In activated HMC-1 cells, the expression level of NF-kappaB/Rel A protein increased in the nucleus, whereas the level of NF-kappaB/Rel A in the nucleus was decreased by AAS treatment. In addition, AAS inhibited the PMACI-induced IkappaBalpha degradation. In conclusion, the present results indicate that AAS has potent anti-anaphylactic and anti-inflammatory properties.
Cancer Preventive Material Development Research Center, Department of Pharmacology, Institute of Oriental Medicine, College of Oriental Medicine, Kyung Hee University, Kyung Hee, South Korea.
Tae-Hee
TH
Kang
In-Young
IY
Choi
Su-Jin
SJ
Kim
Phil-Dong
PD
Moon
Jae-Uk
JU
Seo
Jae-Joong
JJ
Kim
Nyeon-Hyung
NH
An
Sung-Hoon
SH
Kim
Min-Ho
MH
Kim
Jae-Young
JY
Um
Seung-Heon
SH
Hong
Hyung-Min
HM
Kim
Hyun-Ja
HJ
Jeong
D032268:Ailanthus / Q000737:chemistry*; D000707:Anaphylaxis / Q000188:drug therapy* / Q000276:immunology*; D000818:Animals; D016207:Cytokines / Q000096:biosynthesis*; D004487:Edema / Q000473:pathology; D006636:Histamine Release / Q000187:drug effects; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D008407:Mast Cells / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D008813:Mice, Inbred ICR; D016328:NF-kappa B / Q000378:metabolism*; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D003189:p-Methoxy-N-methylphenethylamine
D016207:Cytokines; D018836:Inflammation Mediators; D016328:NF-kappa B; D010936:Plant Extracts; D003189:p-Methoxy-N-methylphenethylamine