肿瘤坏死因子- α和糖皮质激素在硫酸肼介导的抗内毒素致死保护中的作用。

Circulatory shock Pub Date : 1994-05-01
D C Johnson, M A Freudenberg, F Jia, J C Gonzalez, C Galanos, D C Morrison, R Silverstein
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引用次数: 0

摘要

在我们的实验室中,硫酸肼预处理已经被证明可以保护正常小鼠免受内毒素的侵害,而d -半乳糖胺致敏小鼠则可以保护外源性肿瘤坏死因子(TNF)和内毒素。完整的脑下垂体是保护作用的表现。此外,我们已经证明,硫酸肼预处理特异性调节TNF对体外小鼠巨噬细胞脂多糖(LPS)的反应。这项体内研究是为了测试TNF反应的降低和/或糖皮质激素反应的增加是否有助于硫酸肼抵抗lps诱导的体内致死。本研究的结果表明,硫酸肼预处理可选择性地降低LPS刺激后的循环TNF水平。此外,肾上腺切除术取消了硫酸肼的保护作用,但并不能阻止硫酸肼对LPS的循环TNF水平的衰减。然而,皮质酮可恢复硫酸肼介导的保护作用。因此,硫酸肼保护肾上腺切除小鼠免受LPS致死的机制包括内毒素对TNF的调节,以及对糖皮质激素的关键需求。
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Contribution of tumor necrosis factor-alpha and glucocorticoid in hydrazine sulfate-mediated protection against endotoxin lethality.

Hydrazine sulfate pretreatment has previously been shown in our laboratory to protect normal mice against endotoxin and D-galactosamine-sensitized mice against both exogenous tumor necrosis factor (TNF) and endotoxin. An intact pituitary is required for manifestation of the protective effects. Further, we have demonstrated that hydrazine sulfate pretreatment specifically modulates the TNF response to lipopolysaccharide (LPS) in mouse macrophages in vitro. This in vivo study was performed to test whether a reduced TNF response and/or increased glucocorticoid response may contribute to hydrazine sulfate protection against LPS-induced lethality in vivo. The results presented here establish that hydrazine sulfate pretreatment selectively attenuates circulating TNF levels following LPS challenge. Moreover, adrenalectomy abrogates hydrazine sulfate protection but does not prevent hydrazine sulfate attenuation of circulating TNF levels in response to LPS. Hydrazine sulfate-mediated protection is, however, restored permissively by corticosterone. Thus, the mechanism by which hydrazine sulfate protects against LPS lethality in adrenalectomized mice includes TNF modulation in response to endotoxin, as well as a pivotal requirement for glucocorticoid.

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