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长期持续暴露于静磁场可降低多糖诱导的成纤维细胞毒性。

Long-term continuous exposure to static magnetic field reduces popolysaccharide-induced cytotoxicity of fibroblasts.

作者信息

Lin Che-Tong, Lee Sheng-Yang, Chen Chun-Yang, Chen Chi-An, Lin Chih-Ping, Huang Haw-Ming

机构信息

School of Dentistry, Taipei Medical University, Taiwan.

出版信息

Int J Radiat Biol. 2008 Mar;84(3):219-26. doi: 10.1080/09553000801902158.

DOI:10.1080/09553000801902158
PMID:18300022
Abstract

PURPOSES

Lipopolysaccharide (LPS) is one of the major substances initiating the immune host response in microbial infections that results in cytotoxicity. In terms of treatment of the immune response, research has been conducted on physical environments that can reduce LPS-induced damage. In this experiment, a long-term continuous static magnetic field (SMF) was used as a physical resource to reduce LPS-induced immune host response.

MATERIALS AND METHODS

Cultured fibroblasts were challenged with LPS to initiate an inflammatory reaction. Cell viability and various proinflammatory cytokine levels were detected and compared between SMF and sham-exposed groups.

RESULTS

Our in vitro study revealed that, with LPS challenge, fibroblasts continuously exposed to a 0.4-T SMF for 12 h demonstrated higher cell viability compared to unexposed analogs. From cytokine test, the levels of LPS-induced interleukin-1beta (IL-1beta) in the SMF-exposed groups were significantly lower relative to their unexposed counterparts (p < 0.05). By contrast, SMF exposure tended to increase the level of LPS-induced IL-1 receptor antagonist (IL-1Ra) and IL-6.

CONCLUSIONS

Our results suggest that SMF stimulation inhibits LPS-induced cytotoxicity through reduction of proinflammatory cytokines and increase in anti-inflammatory cytokines of NIH-3T3 cells.

摘要

目的

脂多糖(LPS)是引发微生物感染中免疫宿主反应并导致细胞毒性的主要物质之一。在免疫反应治疗方面,已针对可减少LPS诱导损伤的物理环境展开研究。在本实验中,长期连续静磁场(SMF)被用作一种物理资源来减轻LPS诱导的免疫宿主反应。

材料与方法

用LPS刺激培养的成纤维细胞以引发炎症反应。检测并比较了SMF组和假暴露组的细胞活力及多种促炎细胞因子水平。

结果

我们的体外研究表明,在LPS刺激下,连续12小时暴露于0.4-T SMF的成纤维细胞与未暴露的同类细胞相比,具有更高的细胞活力。从细胞因子检测结果来看,与未暴露组相比,暴露于SMF组中LPS诱导的白细胞介素-1β(IL-1β)水平显著降低(p < 0.05)。相比之下,暴露于SMF往往会增加LPS诱导的白细胞介素-1受体拮抗剂(IL-1Ra)和白细胞介素-6的水平。

结论

我们的结果表明,SMF刺激通过降低促炎细胞因子并增加NIH-3T3细胞的抗炎细胞因子来抑制LPS诱导的细胞毒性。

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