AVEMAR (a new benzoquinone-containing natural product) administration interferes with the Th2 response in experimental SLE and promotes amelioration of the disease

被引:23
作者
Ehrenfeld, M
Blank, M
Shoenfeld, Y [1 ]
Hidvegi, M
机构
[1] Tel Aviv Univ, Sackler Fac Med, Chaim Sheba Med Ctr, Ctr Autoimmune Dis,Dept Med B, IL-52621 Tel Hashomer, Israel
[2] Budapest Univ Technol & Econ, Dept Biochem & Food Technol, Budapest, Hungary
关键词
AVEMAR; benzoquinone; wheat germ; experimental model; autoantibodies; cytokines;
D O I
10.1191/096120301682430203
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The potential of oral treatment with AVEMAR (AVEMAR), a new benzoquinone- containing fermentation product of wheat germ, on features of experimental systemic lupus erythematosus (SLE) in naive mice, induced by idiotypic manipulation, was studied. We assessed the effect of AVEMAR on the profile of autoantibody production and the response of Th1/Th2 related cytokines as well as the clinical picture of experimental SLE in the SLE-induced mice. When the product was given in the pre-immunization period, down-regulation of autoantibody production (anti-dsDNA, mouse 16/6 Id, and anti-histones) following treatment with AVEMAR was noted (eg anti-dsDNA decreased from 0.898 +/- 0.097 OD at 405 nm to 0.519 +/- 0.103 OD following treatment). This effect was sustained for at least 4 weeks after discontinuation of the therapy. Serological manifestations associated with a delay in Th2 response (IL-4 and IL-10) were recorded (eg IL-4 decreased from 91.7 +/- 8.11 to 59.55 +/- 7.78ng/ml in splenocyte condition media). The mice showed normal ESR, WBC and less than 100 mg/dl of protein in the urine in comparison to > 300 mg/dl protein in the SLE non-treated mice. In conclusion, oral intake of AVEMAR can ameliorate the clinical manifestations of experimental SLE, via affecting the Th1/Th2 network inhibiting Th2 response.
引用
收藏
页码:622 / 627
页数:6
相关论文
共 45 条
[1]   INDUCTION OF PRIMARY ANTIPHOSPHOLIPID SYNDROME IN MICE BY IMMUNIZATION WITH A HUMAN MONOCLONAL ANTICARDIOLIPIN ANTIBODY (H-3) [J].
BAKIMER, R ;
FISHMAN, P ;
BLANK, M ;
SREDNI, B ;
DJALDETTI, M ;
SHOENFELD, Y .
JOURNAL OF CLINICAL INVESTIGATION, 1992, 89 (05) :1558-1563
[2]  
BLANK M, 1995, CLIN EXP IMMUNOL, V102, P120
[3]   INDUCTION OF SLE-LIKE DISEASE IN NAIVE MICE WITH A MONOCLONAL ANTI-DNA ANTIBODY DERIVED FROM A PATIENT WITH POLYMYOSITIS CARRYING THE 16/6 ID [J].
BLANK, M ;
MENDELOVIC, S ;
MOZES, E ;
SHOENFELD, Y .
JOURNAL OF AUTOIMMUNITY, 1988, 1 (06) :683-691
[4]  
ERICKSON KL, 1992, NUTRITION AND IMMUNOLOGY, P81
[5]  
GERSHWIN ME, 1984, J IMMUNOL, V133, P222
[6]   Disease severity in patients with systemic lupus erythematosus correlates with an increased ratio of interleukin-10:Interferon-gamma-secreting cells in the peripheral blood [J].
Hagiwara, E ;
Gourley, MF ;
Lee, S ;
Klinman, DM .
ARTHRITIS AND RHEUMATISM, 1996, 39 (03) :379-385
[7]  
Hidvégi M, 1998, ANTICANCER RES, V18, P2353
[8]   MSC, a new benzoquinone-containing natural product with antimetastatic effect [J].
Hidvégi, M ;
Rásó, E ;
Tömösközi-Farkas, R ;
Szende, B ;
Paku, S ;
Prónai, L ;
Bocsi, J ;
Lapis, K .
CANCER BIOTHERAPY AND RADIOPHARMACEUTICALS, 1999, 14 (04) :277-289
[9]   Effect of MSC on the immune response of mice [J].
Hidvégi, M ;
Rásó, E ;
Farkas, RT ;
Lapis, K ;
Szende, B .
IMMUNOPHARMACOLOGY, 1999, 41 (03) :183-186
[10]  
Horwitz DA, 1998, ARTHRITIS RHEUM, V41, P838, DOI 10.1002/1529-0131(199805)41:5<838::AID-ART10>3.0.CO