Abstract
Gluracarticoid steroids provide considerable protection against the systemic toxicity or tumor necrosis factor-α (TNF-α, cachexin). In animal experiments RU 38486 (mircpristone), a steroid antagonist, increased the synthesis of TNF and sensitized the animals to the cytotoxic action of TNF. As compared to the control and methylprednisolone-treated groups, mifepristone significantly increased the level of TNF in the serum, liver and spleen or lipopolysaccharide (LPS)-treated animals. In tissue cultures F.U. 38486 induced the TNF synthesis of mycloid cells and increase the TNF production or genetically modified HeLa cells, which synthesize TNF constitutively. Normal and tumor cell cultures exhibited increased sensitivity toward TNF in the presence of mifepristone.
Highlights
Tumor necrosis factor (TNF) shows a very high spccif’lti:yinits cytotoxicity towards ccrtnin tumor cells [l]
TNF.a is il mucrophugedcrivcd peptids hormone rclcoscd in response to different stimuli. in= eluding bacteria! LPS. It has !xcn implicated as u prin. ciptl! mediator in septic and cndotoain shock
In in vitro models. glucocorticoids inhibit the synthesis of TNF and another important septic shock mediator
Summary
Tumor necrosis factor (TNF) shows a very high spccif’lti:yinits cytotoxicity towards ccrtnin tumor cells [l]. Glucocorticoid hormones arc krlown to protect cxgcrimcntal animals very cffcctivcly against the lethal effect of bacterial cndotoxins [a], but the bcncficial influcncc of these hormones in clinical and cxpcrimcntol fomls of septic shock remains a question of d&ate [9-l I]. Glucocorticoids inhibit LDS.induced TNF production [19] and TNF can stimulate pituitary adrcnocorticotropin secretion, resulting in the rclcasc of corticostcrone [20,:!1].All thcsc findings suggest an important role of the ncurocndocrinc axis in the secretion of steroid hormones and in the modulation of cytokinc production. On this basis, WCset out to study the influence of RU 38486 on TNF production and toxicity
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