Begon Sophie, Alloui Abdelkrim, Eschalier Alain, Mazur André, Rayssiguier Yves, Dubray Claude
INSERM EMI 9904-Pharmacologie Fondamentale et Clinique de la Douleur, Laboratoire de Pharmacologie Médicale, Faculté de Médecine, Clermont-Ferrand, France.
Life Sci. 2002 Jan 18;70(9):1053-63. doi: 10.1016/s0024-3205(01)01475-8.
Magnesium-deficient rats develop simultaneously a significant lowering of nociceptive threshold and a generalized inflammation. We investigated the relationship between these two phenomena by testing drugs that are able to suppress the inflammation in this model. In weaning rats fed a magnesium-depleted diet for ten days, the nociceptive threshold was assessed by the paw pressure test and the inflammation by a clinical score. A non-steroidal anti-inflammatory drug (piroxicam); antagonists of H1 and H2 receptors (astemizole and cimetidine. respectively); a glucocorticoid (dexamethasone); an inhibitor of mastocyte degranulation (cromoglycate); and estradiol benzoate were used to block the inflammatory response. Dexamethasone and estradiol significantly suppressed the inflammation (p < 0.001 vs control group). Cromoglycate showed a delayed anti-inflammatory effect (p < 0.01 vs control group on D10). The combination of astemizole and cimetidine partially blocked the inflammation process, whereas astemizole and piroxicam were without effect. Regardless of the effect of the test drugs on inflammation, no change in the time course of hyperalgesia was observed. These data support the view that hyperalgesia induced by the magnesium-depleted diet is not a consequence of the inflammatory process.
缺镁大鼠会同时出现痛觉阈值显著降低和全身性炎症。我们通过测试能够抑制该模型炎症的药物来研究这两种现象之间的关系。在断奶大鼠中，给予缺镁饮食十天，通过爪部压力测试评估痛觉阈值，通过临床评分评估炎症。使用一种非甾体抗炎药（吡罗昔康）、H1和H2受体拮抗剂（分别为阿司咪唑和西咪替丁）、一种糖皮质激素（地塞米松）、一种肥大细胞脱颗粒抑制剂（色甘酸）以及苯甲酸雌二醇来阻断炎症反应。地塞米松和雌二醇显著抑制了炎症（与对照组相比，p < 0.001）。色甘酸显示出延迟的抗炎作用（在第10天与对照组相比，p < 0.01）。阿司咪唑和西咪替丁的组合部分阻断了炎症过程，而阿司咪唑和吡罗昔康则没有效果。无论测试药物对炎症的影响如何，均未观察到痛觉过敏时间进程的变化。这些数据支持这样一种观点，即缺镁饮食诱导的痛觉过敏不是炎症过程的结果。
