Bonamin L V, Martinho K S, Nina A L, Caviglia F, Do Rio R G
Faculty of Veterinary Medicine, University of Santo Amaro, São Paulo, Brazil.
Br Homeopath J. 2001 Oct;90(4):198-203. doi: 10.1054/homp.1999.0496.
We evaluated the interaction of dexamethasone 10(-17) and 10(-33) M (equivalent to 7cH and 15cH) with dexamethasone in pharmacological concentrations, using as experimental models: acute inflammation induced by carrageenan, Ehrlich ascitic tumour, and migration of tumour infiltrating leukocytes (TIL). Male adult BALB/c mice (n=7 per group) were used in all experiments. Carrageenan (1%) was injected into the footpad for oedema evaluation and into the peritoneal cavity (i.p.), for differential counting of inflammatory cells. Ehrlich ascitic tumour cells (10(7) viable cells/ml) were injected i.p. and tumour cells were counted after 6 days, by the Trypan blue exclusion method. The differential TIL was counted using smears stained by hematoxylin-eosin. Treatments were made immediately after carrageenan inoculation or once a day, during Ehrlich tumour development, until the animals were killed. Animals were treated with the following preparations: (1) phosphate buffer saline (PBS) solution; (2) dexamethasone (0.5 mg/kg for inflammation model or 4mg/kg for tumour model) mixed with dexamethasone 7cH or 15cH; (3) dexamethasone (same doses) mixed in PBS. Homeopathic dexamethasone partially blocked the anti-inflammatory effect of pharmacological dexamethasone with regard to paw oedema (two-way ANOVA, P < 0.0008) and polymorphonuclear cell migration (chi2, P=0.0001). No important differences were observed between experimental and control groups, in relation to Ehrlich tumour cells viability or count, or bodyweight, but potentised dexamethasone restored control levels of TIL viability, compared to mice treated with pharmacological doses of dexamethasone (chi2, P< or = 0.001). The results demonstrate that a potentised substance may change its own pharmacological effects and suggest that ultradilutions effects act mostly on host response.
我们以角叉菜胶诱导的急性炎症、艾氏腹水瘤以及肿瘤浸润白细胞（TIL）迁移为实验模型，评估了10⁻¹⁷M和10⁻³³M（相当于7cH和15cH）的地塞米松与药理浓度的地塞米松之间的相互作用。所有实验均使用成年雄性BALB/c小鼠（每组n = 7）。将1%的角叉菜胶注射到足垫用于评估水肿，注射到腹腔（i.p.）用于炎症细胞的差异计数。将艾氏腹水瘤细胞（10⁷个活细胞/ml）经腹腔注射，6天后通过台盼蓝排斥法对肿瘤细胞进行计数。使用苏木精 - 伊红染色的涂片对TIL进行差异计数。在接种角叉菜胶后立即进行处理，或者在艾氏肿瘤发展期间每天处理一次，直至处死动物。动物接受以下制剂处理：（1）磷酸盐缓冲盐水（PBS）溶液；（2）地塞米松（炎症模型为0.5mg/kg，肿瘤模型为4mg/kg）与地塞米松7cH或15cH混合；（3）地塞米松（相同剂量）与PBS混合。顺势疗法的地塞米松在爪部水肿方面（双向方差分析，P < 0.0008）和多形核细胞迁移方面（χ²，P = 0.0001）部分阻断了药理剂量地塞米松的抗炎作用。在艾氏肿瘤细胞活力或计数以及体重方面，实验组和对照组之间未观察到重要差异，但与用药理剂量地塞米松处理的小鼠相比，增效地塞米松恢复了TIL活力的对照水平（χ²，P ≤ 0.001）。结果表明，一种增效物质可能会改变其自身的药理作用，并提示超稀释效应主要作用于宿主反应。
