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[二丁酰环磷腺苷对人单核细胞肿瘤坏死因子及白细胞介素-1产生的影响]

[Effects of DbcAMP on tumor necrosis factor and interleukin-1 production in human monocytes].

作者信息

Sato W, Enzan K, Kayaba M, Masaki Y, Matsumoto J, Suzuki M

机构信息

Department of Anesthesiology, Akita University School of Medicine.

出版信息

Masui. 1993 Sep;42(9):1302-5.

PMID:8230718
Abstract

Recent reports have shown that dibutyryl cAMP (DbcAMP) blocks endotoxin-induced lung injury. To determine whether DbcAMP suppresses the production of tumor necrosis factor (TNF) and interleukin-1 (IL-1) in human monocytes, we measured the levels of TNF and IL-1 in response to E. Coli lipopolysaccharide (40 micrograms.ml-1) in vitro. We now show that DbcAMP suppressed dose-dependently the production of TNF in human monocytes, and DbcAMP totally suppressed it at the dose above 5 x 10(-4) M. However, DbcAMP did not suppress the production of IL-1 even at the dose of 5 x 10(-3) M in human monocytes. These data suggest that the productive mechanism of IL-1 may be different from that of TNF. Further, suppression of TNF by DbcAMP may contribute to the beneficial effects in animal models of septic shock or lung injury and this may have clinical implications.

摘要

最近的报告显示,二丁酰环磷腺苷(DbcAMP)可阻止内毒素诱导的肺损伤。为了确定DbcAMP是否抑制人单核细胞中肿瘤坏死因子(TNF)和白细胞介素-1(IL-1)的产生,我们在体外测量了对大肠杆菌脂多糖(40微克/毫升)反应时TNF和IL-1的水平。我们现在表明,DbcAMP剂量依赖性地抑制人单核细胞中TNF的产生,并且在高于5×10^(-4)M的剂量下DbcAMP完全抑制了它。然而,即使在5×10^(-3)M的剂量下,DbcAMP也不抑制人单核细胞中IL-1的产生。这些数据表明IL-1的产生机制可能与TNF不同。此外,DbcAMP对TNF的抑制可能有助于在脓毒症休克或肺损伤动物模型中产生有益作用,这可能具有临床意义。

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