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镉的促炎特性。

Pro-inflammatory properties of cadmium.

作者信息

Olszowski Tomasz, Baranowska-Bosiacka Irena, Gutowska Izabela, Chlubek Dariusz

机构信息

Department of Hygiene, Pomeranian Medical University, Szczecin, Poland.

出版信息

Acta Biochim Pol. 2012;59(4):475-82. Epub 2012 Dec 13.

PMID:23240106
Abstract

Cadmium is a toxic and carcinogenic heavy metal that nowadays constitutes a serious environmental health problem. The aim of this study is to review the effects of cadmium on selected inflammatory mediators and markers, such as NF-κB and AP-1 transcription factors, IL-6, TNF-α, IL-1β cytokines, IL-8 or MIP-2 chemokine, MPO, iNOS, MMPs and COX-2 enzymes, PGE(2) (product of COX-2 enzyme), ICAM-1, VCAM-1 and PECAM-1 adhesion molecules, and CRP. The research strategy identified articles available in Medline, published between 1998 and 2012; we included both in vivo and in vitro studies carried out on humans and rodents. Most of the reviewed research findings suggest that cadmium in micromolar concentrations (especially in the 1-10 μM range) causes up-regulation of the mediators and markers of inflammation, and appears to have pro-inflammatory properties. However, it is worth mentioning that a contradictory or even opposite hypothesis exists, which suggests cadmium to be an anti-inflammatory factor. Further research including detailed histological analyses should solve this discrepancy. Nevertheless, it appears that the main reason for these contradictory findings is the experimental setup: different biological systems analyzed and different doses of cadmium applied.

摘要

镉是一种有毒的致癌重金属,如今已构成严重的环境卫生问题。本研究的目的是综述镉对某些炎症介质和标志物的影响,如核因子-κB(NF-κB)和活化蛋白-1(AP-1)转录因子、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)细胞因子、白细胞介素-8(IL-8)或巨噬细胞炎性蛋白-2(MIP-2)趋化因子、髓过氧化物酶(MPO)、诱导型一氧化氮合酶(iNOS)、基质金属蛋白酶(MMPs)和环氧化酶-2(COX-2)、前列腺素E2(PGE2,COX-2酶的产物)、细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)和平板内皮细胞黏附分子-1(PECAM-1)以及C反应蛋白(CRP)。研究策略确定了1998年至2012年间发表在医学在线数据库(Medline)上的文章;我们纳入了对人类和啮齿动物进行的体内和体外研究。大多数综述研究结果表明,微摩尔浓度的镉(尤其是在1-10μM范围内)会导致炎症介质和标志物的上调,并且似乎具有促炎特性。然而,值得一提的是,存在一个矛盾甚至相反的假设,即认为镉是一种抗炎因子。包括详细组织学分析在内的进一步研究应能解决这一差异。尽管如此,这些矛盾结果的主要原因似乎在于实验设置:所分析的不同生物系统以及所应用的不同镉剂量。

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