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高尿酸血症大鼠中佐剂诱导性关节炎的抑制作用

Inhibition of adjuvant-induced arthritis in the hyperuricemic rat.

作者信息

Lussier A, de Medicis R, Marquis L, Menard H

出版信息

Agents Actions. 1978 Oct;8(5):536-42. doi: 10.1007/BF02111442.

Abstract

In man, there is a strong negative correlation between gout and rheumatoid arthritis. To investigate this apparent mutual exclusion, we studied the influence of oxonate-induced hyperuricemia on the development of adjuvant arthritis in male Wistar rats. The results indicate that in the primary reaction (inflammation of the injected paw) the differences are weak (0.10 greater than p greater than 0.05) between normouricemic and hyperuricemic rats. In hyperuricemic rats the secondary reaction (induced polyarthritis) is delayed and significantly reduced (p less than 0.005). Non-immunologic carrageenin paw edema is not statistically different between the two groups (p greater than 0.25). Experimental hyperuricemia in rats seems to influence essentially the secondary, cell mediated, reaction without affecting the acute inflammatory phases.

摘要

在人类中,痛风与类风湿性关节炎之间存在强烈的负相关。为了研究这种明显的相互排斥关系,我们研究了氧嗪酸钾诱导的高尿酸血症对雄性Wistar大鼠佐剂性关节炎发展的影响。结果表明,在初级反应(注射爪的炎症)中,正常尿酸血症大鼠和高尿酸血症大鼠之间的差异较小(0.10>p>0.05)。在高尿酸血症大鼠中,次级反应(诱导性多关节炎)延迟且显著减轻(p<0.005)。两组之间非免疫性角叉菜胶爪肿胀无统计学差异(p>0.25)。大鼠实验性高尿酸血症似乎主要影响次级的细胞介导反应,而不影响急性炎症阶段。

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