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作 者:蔡定芳[1] 沈时谋 陈晓红[1] 沈自尹[1] 张玲娟 刘彦芳[1]
出 处:《中国中西医结合杂志》1998年第1期4-7,共4页Chinese Journal of Integrated Traditional and Western Medicine
基 金:卫生部科学研究基金!(No94-1-186);上海市科学技术基金!(No9309-7)
摘 要:目的:研究仙灵脾对外源性糖皮质激素抑制下丘脑-垂体-肾上腺-胸腺(HPAT)轴作用的保护效应。方法:临床选择需用强的松治疗的患者65例,随机分为复方强的松组(强的松与仙灵脾合方)与强的松组,观察用药前后皮质醇和促肾上腺皮质激素(ACTH)及淋巴细胞增殖反应的变化;动物实验用皮质酮皮下注射造成大鼠 HPAT轴抑制模型,观察仙灵脾对 HPAT轴相关指标的影响。结果:血浆 ACTH、皮质醇和淋巴细胞增殖反应两组患者治疗前均无明显差异,治疗后强的松组明显下降,复方强的松组明显上升( P< 0. 05)。实验动物表现为下丘脑单胺类递质被激活;垂体、肾上腺、胸腺重量减轻;室旁核、正中隆起 CRH神经细胞与神经纤维减少,肾上腺束状带与胸腺皮质萎缩;自然杀伤细胞细胞毒活性及淋巴细胞产生IL-2、γ-干扰素水平降低(P<0.05);仙灵脾组上述各项指标较皮质酮组明显改善(P<0.05)。结论:仙灵脾具有减轻外源性糖皮质激素副作用的神经内分泌免疫学效应。Objective: To study protective effect of Epimedium brevicornum (EB) on hypothalamus-pituitary- adrenalthymus (HPAT) axis inhibited by exogenous glucocorticoid. Methods: In clinical research, variatoin of cortisol, adrenocorticotrophin (ACTH), lymphocyte proliferative reaction were observed before and after medication in 65 patients took prednisone, and were randomly divided into Fufang prednisone group (mixture of prednisone and EB) and prednison group. An experimental model of HPAT axis inhibited by corticosterone (CORT) was established to observe the effect of EB on relevant indices of HPAT axis. Results: The level of ACTH and CORT in plasma decreased and lymphocyte proliferative reaction reduced in patients (P < 0.05 ). In experimental study, monoaminic transmitters activated in hypothalamus; weight of pituitary, adrenal and thymus decreased; number of CRH positive neurons in hypothalamic paraventricular nucleus, CRH positive neurofibrilin median eminence and anterior pituitary ACTH positive secretory cells decreased; adrenal fasciculate sone and thymus cortex atrophies; NK cell cytotoxicity and the level of IL-2 and γ-IFN which were prepuced by lymphocytes reduced in CORT-rats (P< 0. 05). There were significant difference between Fufang prednisone group (clinical research) or EB group (experimental research) and CORT control groups, P< 0. 05. Conclusion: EB could relieve neuroendocrino-immunological effect inhibited by exogenous glucoclorticoid.
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