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用中药补中益气汤(日语名称:补中益气汤)治疗的小鼠中IgE产生的抑制作用

Suppression of IgE production in mice treated with a traditional Chinese medicine, bu-zhong-yi-qi-tang (Japanese name: hochu-ekki-to).

作者信息

Kaneko M, Kishihara K, Kawakita T, Nakamura T, Takimoto H, Nomoto K

机构信息

Kampo Research Laboratories, Kanebo Co. Ltd., Osaka, Japan.

出版信息

Immunopharmacology. 1997 Apr;36(1):79-85. doi: 10.1016/s0162-3109(96)00162-2.

DOI:10.1016/s0162-3109(96)00162-2
PMID:9129999
Abstract

The ability of a traditional herbal medicine, Bu-zhong-yi-qi-tang (Japanese name: Hochu-ekki-to, HOT), to suppress IgE production was investigated. BALB/c mice were intraperitoneally immunized with aluminium hydroxide adsorbed with DNP-KLH (DNP-KLH + alum). When oral administration of HOT was begun just after immunization, the serum level of antigen-specific IgE was significantly decreased, although those of antigen-specific IgG1 and IgG2a were not influenced. In the culture of spleen cells obtained 14 days after immunization with DNP-KLH, antigen-specific IgE and IgG1 production by the cells of the HOT-treated mice was significantly suppressed compared to that in immunized mice. Furthermore, in the combination culture with CD4+ T cells and B cells separated from spleen cells, IgE production by the cells from immunized mice was inhibited by replacement of their corresponding cell population with either CD4+ T cells or B cells of HOT-treated mice. Additionally, production of interleukin 2 (IL-2) and IL-4 was significantly suppressed in HOT-treated mice but not that of IFN-gamma in comparison to the immunized mice. These results suggested that HOT decreased the IgE level in serum by inhibiting the development of IL-4-producing CD4+ T cells.

摘要

研究了传统草药补中益气汤(日语名称:Hochu-ekki-to,HOT)抑制IgE产生的能力。用吸附有DNP-KLH(DNP-KLH + 明矾)的氢氧化铝对BALB/c小鼠进行腹腔免疫。免疫后立即开始口服HOT,抗原特异性IgE的血清水平显著降低,而抗原特异性IgG1和IgG2a的血清水平不受影响。在用DNP-KLH免疫14天后获得的脾细胞培养物中,与免疫小鼠相比,HOT处理小鼠的细胞产生的抗原特异性IgE和IgG1显著受到抑制。此外,在与从脾细胞中分离出的CD4+ T细胞和B细胞的联合培养中,用HOT处理小鼠的CD4+ T细胞或B细胞替代免疫小鼠的相应细胞群体,可抑制免疫小鼠细胞产生IgE。另外,与免疫小鼠相比,HOT处理小鼠中白细胞介素2(IL-2)和IL-4的产生显著受到抑制,但干扰素-γ的产生不受影响。这些结果表明,HOT通过抑制产生IL-4的CD4+ T细胞的发育来降低血清中的IgE水平。

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