Inhibition of TNF-α, IL-1β, and IL-6 productions and NF-κB activation in lipopolysaccharide-activated RAW 264.7 macrophages by catalposide, an iridoid glycoside isolated ftom Catalpa ovata G. Don (Bignoniaceae)

被引:89
作者
An, SJ
Pae, HO
Oh, GS
Choi, BM
Jeong, S
Jang, SI
Oh, H
Kwon, TO
Song, CE
Chung, HT [1 ]
机构
[1] Wonkwang Univ Sch Med, Dept Microbiol & Immunol, Iksan 570749, Chunbug, South Korea
[2] Wonkwang Univ, MRRC, Iksan 570749, Chunbug, South Korea
[3] Wonkwang Univ, Profess Grad Sch Oriental Med, Iksan 570749, Chunbug, South Korea
[4] Korea Inst Sci & Technol, Div Life Sci, Seoul 130650, South Korea
关键词
LPS; TNF-alpha; IL-1; beta; IL-6; NF-kappa B; catalposide; Catalpa ovata;
D O I
10.1016/S1567-5769(02)00085-1
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Catalposide, the major iridoid glycoside isolated from the stem bark of Catalpa ovata G. Don (Bignoniaceae), was found to inhibit the productions of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6), and the activation of nuclear factor kappaB (NF-kappaB) in RAW 264.7 macrophages activated with lipopolysaccharide (LPS). Catalposide also inhibited the expressions of TNF-alpha, IL-1beta, and IL-6 genes and the nuclear translocation of p65 subunit of NF-kappaB in LPS-activated RAW 264.7 cells. Flow cytometric analysis revealed that catalposide suppressed the binding of FITC-conjugated LPS to CD 14 on the surface of cells, probably resulting in the inhibitory effects on TNT-alpha, IL- 1beta, and IL-6 productions and NF-kappaB activation. These findings suggest that catalposide could be an attractive candidate for adjunctive therapy in Gram-negative bacterial infections. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:1173 / 1181
页数:9
相关论文
共 25 条
[1]   IC14, a CD14 specific monoclonal antibody, is a potential treatment for patients with severe sepsis [J].
Axtelle, T ;
Pribble, J .
JOURNAL OF ENDOTOXIN RESEARCH, 2001, 7 (04) :310-314
[2]  
BURRELL R, 1994, CIRC SHOCK, V43, P137
[3]   GRAM-NEGATIVE BACTERIAL SEPSIS AND SEPSIS SYNDROME [J].
DUNN, DL .
SURGICAL CLINICS OF NORTH AMERICA, 1994, 74 (03) :621-635
[4]  
FREUDENBERG MA, 1993, IMMUN INFEKT, V21, P40
[5]   MECHANISMS OF ENDOTOXIN-SHOCK AND ENDOTOXIN HYPERSENSITIVITY [J].
GALANOS, C ;
FREUDENBERG, MA .
IMMUNOBIOLOGY, 1993, 187 (3-5) :346-356
[6]   Anti-inflammatory glycoterpenoids from Scrophularia auriculata [J].
Giner, RM ;
Villalba, ML ;
Recio, MC ;
Máñez, S ;
Cerdá-Nicolás, M ;
Ríos, JL .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2000, 389 (2-3) :243-252
[7]   MEDIATORS OF SEPTIC SHOCK - NEW APPROACHES FOR INTERRUPTING THE ENDOGENOUS INFLAMMATORY CASCADE [J].
GIROIR, BP .
CRITICAL CARE MEDICINE, 1993, 21 (05) :780-789
[8]   The inflammatory cytokines - New developments in the pathophysiology and treatment of septic shock [J].
Glauser, MP .
DRUGS, 1996, 52 :9-17
[9]   LPS induction of gene expression in human monocytes [J].
Guha, M ;
Mackman, N .
CELLULAR SIGNALLING, 2001, 13 (02) :85-94
[10]   Innate immunity and inflammation: A transcriptional paradigm [J].
Hawiger, J .
IMMUNOLOGIC RESEARCH, 2001, 23 (2-3) :99-109