右归丸对糖皮质激素诱导小鼠胸腺树突状细胞表型变化的作用

作者	单位
周宪宾	山东省医学科学院基础所山东省医药卫生肿瘤免疫与中药免疫重点实验室济南250062
王丽	山东省医学科学院基础所山东省医药卫生肿瘤免疫与中药免疫重点实验室济南250062
郭钰琪	山东省医学科学院基础所山东省医药卫生肿瘤免疫与中药免疫重点实验室济南250062
姚成芳	山东省医学科学院基础所山东省医药卫生肿瘤免疫与中药免疫重点实验室济南250062

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中文摘要:

目的探讨糖皮质激素对小鼠胸腺树突状细胞表型的影响以及中药右归丸的保护作用。方法BALB/c小鼠经肌肉注射氢化可的松(10mg/kg)或联合灌胃右归丸(20.81g/kg)处理,肌肉注射或灌胃等量生理盐水处理的小鼠作为对照组,采用流式细胞术检测处理小鼠胸腺树突状细胞(CD11c+CD45+)抗原递呈分子(H-2Kd、I-Ad)的变化;同时采用RT-PCR法检测胸腺细胞细胞间黏附分子-1(ICAM-1)及淋巴细胞功能相关抗原-1 LFA-1 mRNA的表达。结果与对照组〔CD11c+I-Ad+树突状细胞比例(65.81±7.69)%,CD11c+H-2Kd+细胞比例(31.88±5.01)%〕比较,氢化可的松组小鼠胸腺CD11c+I-Ad+树突状细胞比例〔(46.77±4.32)%〕显著降低(P<0.01),CD11c+H-2Kd+细胞比例〔(64.34±7.69)%〕升高(P<0.01);同时,氢化可的松组胸腺细胞中ICAM-1及LFA-1 mRNA表达〔(30.11±2.51)%,(30.40±3.77)%〕下降,与对照组〔(46.35±3.34)%,(47.28±2.91)%〕比较,差异有统计学意义(P<0.01);氢化可的松+右归丸能显著逆转糖皮质激素诱导的I-Ad+树突状细胞比例〔(54.19±5.08)%〕下降,上调胸腺细胞ICAM-1及LFA-1 mRNA表达〔(33.97±2.04)%,(34.80±2.92)%〕,与氢化可的松组比较,差异有统计学意义(P<0.05)。结论糖皮质激素可抑制小鼠胸腺CD11c+CD45+树突状细胞MHC-Ⅱ类分子I-Ad表达,上调该群细胞MHC-Ⅰ类分子H-2Kd的表达,同时下调相关黏附分子ICAM-1及LFA-1的转录,而补阳方剂右归丸对激素诱导的MHC-Ⅱ分子下调和黏附分子转录水平下降有显著的抑制作用。

英文摘要:

ObjectiveTo investigate the influence of glucocorticoid on phenotype of thymic dendritic cells in mice and to investigate the protective effect of Yougui Pill(YGP) on it.MethodsBALB/c mice allocated in the group A and B were treated respectively with 10 mg/kg hydrocortisone,alone and combined with 20.81 g/kg YGP.The control mice were treated with normal saline.The changes before and after treatment of I-Ad and H-2Kd antigen presentation molecules expression in CD11c+ and CD45+ thymic dendritic cells of mice were analyzed by flow cytometry assay,and the expression of intercellular adhesion molecule-1(ICAM-1) and leukocyte function-associated antigen-1(LFA-1) mRNA in thymocytes were determined by RT-PCR as well.ResultsThe percentage of I-Ad+ and H-2Kd+ in CD11c+ in Group A after treatment was 46.77±4.32% and 64.34±7.69% respectively,as compared with those in the control group(65.81±7.69% and 31.88±5.01%),the percentage of I-Ad+ was lower and that of H-2Kd+ was higher significantly(all P<0.01).Meantime,the expression of ICAM-1 and LFA-1 in thymocyte in Group A(30.11±2.51% and 30.40±3.77%) was significantly lower than that in the control group(46.35±3.34% and 47.28±2.91%) respectively(P<0.01).Changes in Group B showed that treated by hydrocortisone in combination with YGP,the above-mentioned hydrocortisone-induced changes could be obviously reversed,the outcome of CD11c+I-Ad+ was 54.19±5.08%,ICAM-1 33.97±2.04% and LFA-1 34.80±2.92%,the difference between the two treated groups in these indexes all showed statistical significance(P<0.05).ConclusionGlucocorticoid can inhibit the expression of major histocompatibility complex class Ⅱ antigen molecule,but promote the expression of major histocompatibility complex class Ⅰ in CD11c+ and CD45+ dendritic cells,down-regulate ICAM-1 and LFA-1 transcription,while the tonifying yang recipe,YGP,has a dominant protective effect against the above actions of glucocorticoid.

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