摘要
目的：观察乌头碱（ＡＴＮ）对正常小鼠和皮质酮所致阳虚模型小鼠腹腔巨噬细胞（ＭΦ）在干扰素（ＩＮＦ－γ）诱导下，其表面Ｉａ抗原表达的改变。方法：采用流式细胞技术测定。结果：正常小鼠腹腔注射ＡＴＮ（１．５、３．０和６．０μｇ·ｋｇ－１·ｄ－１）７ｄ后，其ＭΦ在３００Ｕ·Ｌ－１浓度ＩＮＦ－的诱导下Ｉａ抗原表达明显增强，反映Ｉａ抗原表达的荧光强度从对照组的９３．０１±１３．３０增加到１０８．９０±８．６３、１１３．０１±１２．８０和１１３．５７±１０．１３（Ｐ＜０．０５）。阳虚模型小鼠腹腔ＭΦ在ＩＦＮ－诱导下的Ｉａ抗原表达明显低于正常小鼠（９０．８０±７．３６和１０９．９６±１０．３７，Ｐ＜０．０５），但ＡＴＮ治疗可使阳虚模型小鼠ＭΦ的Ｉａ抗原表达增强到１１１．１１±１４．４８、１１７．８９±１４．６４和１１５．６１±１３．７４，与模型组相比差异显著（Ｐ＜０．０５和Ｐ＜０．０１）。结论：说明ＡＴＮ能够提高正常小鼠和皮质酮免疫抑制阳虚模型小鼠ＭΦＩａ抗原的表达，从而增强ＭΦ递呈抗原能力，促进免疫应答反应。
AIM: To study the effect of aconitine (ATN) on peritoneal macrophage Ia expression induced with IFN in both normal mice and “Yang” deficiency mice caused by corticostron. METHOD: Using flow cytometric analysis technic. RESULTS: ①The fluorescent intensity of macrophage Ia expression induced with 300 μg·L -1 IFN in normal mice injected ip. ATN 1 5, 3 0 or 6 0 μg·kg -1 ·d -1 for 7 days were significantly higher than that in control (108 90±8 63,113 01±12 80 and 113 57±10 13 vs. 93 01±13 30, P< 0 05). ② The fluorescent intensity in Yang deficiency mice was significantly lower than that in control (90 80±7 36 vs. 109·96±10 37, P< 0 05), and ATN could significantly increase the fluorescent intensity of Yang deficency mice to 111 11±14 48, 117 89±14 64 and 115 61±13 7 ( P< 0 05, P< 0 01). CONCLUSION: ATN could not only improve the peritoneal macrophage Ia expression induced with IFN in normal mice, but also significantly antagonize the suppressive effect of corticostron on macrophage Ia expression of Yang deficiency mice, and these results implied that ATN could enhance macrophage to present antigen and promote the immune response.
出处
《中国药理学通报》
CAS
CSCD
北大核心
1997年第4期341-344,共4页
Chinese Pharmacological Bulletin
基金
国家教育委员会优秀年轻教师基金
关键词
乌头碱
腹腔巨噬细胞
IA抗原表达
aconitine
macrophage
Ia expression
corticostron
animal model
yang deficiency
