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碱式碳酸镍可增加肺泡巨噬细胞分泌肿瘤坏死因子α和白细胞介素6。

Nickel hydroxy carbonate increases tumour necrosis factor alpha and interleukin 6 secretion by alveolar macrophages.

作者信息

Arsalane K, Gosset P, Hildebrand H F, Voisin C, Tonnel A B, Wallaert B

机构信息

Laboratoire de Pathologie Respiratoire Expérimentale et de Pollution Atmosphérique, Institut Pasteur, Lille, France.

出版信息

J Appl Toxicol. 1994 Sep-Oct;14(5):375-9. doi: 10.1002/jat.2550140510.

Abstract

The aim of the current study was to assess the in vitro effects of nickel hydroxy carbonate (NiHC) at noncytotoxic concentrations on the production of cytokines such as tumour necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) in alveolar macrophages (AMs). The effect of NiHC was evaluated in both unstimulated AMs and cells activated by lipopolysaccharide (LPS). Cytotoxicity was related to lactate dehydrogenase release and ATP cell content. The results confirm that NiHC at concentrations of 0.125, 1.25 and 3.125 micrograms NiHC 10(-6) cells was not cytotoxic. The NiHC exposure of unstimulated AMs significantly increased the release of TNF-alpha at all concentrations and that of IL-6 at 1.25 micrograms NiHC 10(-6) cells. LPS addition significantly increased the secretion of both cytokines. However, NiHC did not cause a significant increase in the release of TNF-alpha and IL-6 in LPS-stimulated cells. In conclusion, the ability of NiHC to activate AMs and to release increased amounts of pro-inflammatory mediators may be responsible, at least partly, for inflammation and pneumotoxicity associated with nickel exposure.

摘要

本研究的目的是评估碳酸羟基镍(NiHC)在无细胞毒性浓度下对肺泡巨噬细胞(AM)中细胞因子产生的体外影响,这些细胞因子包括肿瘤坏死因子α(TNF-α)和白细胞介素6(IL-6)。在未受刺激的AM和由脂多糖(LPS)激活的细胞中评估了NiHC的作用。细胞毒性与乳酸脱氢酶释放和ATP细胞含量相关。结果证实,浓度为0.125、1.25和3.125微克NiHC/10^(-6)个细胞时,NiHC无细胞毒性。未受刺激的AM暴露于NiHC后,在所有浓度下TNF-α的释放均显著增加,在1.25微克NiHC/10^(-6)个细胞时IL-6的释放显著增加。添加LPS显著增加了两种细胞因子的分泌。然而,NiHC并未导致LPS刺激的细胞中TNF-α和IL-6的释放显著增加。总之,NiHC激活AM并释放更多促炎介质的能力可能至少部分地导致了与镍暴露相关的炎症和肺毒性。

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