Long-term continuous exposure to static magnetic field reduces popolysaccharide-induced cytotoxicity of fibroblasts
Long-term continuous exposure to static magnetic field reduces popolysaccharide-induced cytotoxicity of fibroblasts
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DOI：
10.1080/09553000801902158
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发表时间：
2008-03-01
影响因子：
2.6
通讯作者：
Huang, Haw-Ming
中科院分区：
文献类型：
--
作者：
Lin, Che-Tong;Lee, Sheng-Yang;Huang, Haw-Ming
目的：脂多糖（LPS）是微生物感染中引发免疫宿主反应的主要物质之一，导致细胞毒性。在免疫反应的治疗方面，已经对能够减少lps引起的损伤的物理环境进行了研究。本实验采用长时间连续静态磁场（SMF）作为物理资源，降低lps诱导的免疫宿主反应。材料和方法：用LPS刺激培养成纤维细胞引发炎症反应。检测并比较假暴露组和假暴露组的细胞活力和各种促炎细胞因子水平。结果：我们的体外研究显示，与未暴露的类似物相比，在LPS刺激下，连续暴露于0.4 t SMF 12小时的成纤维细胞表现出更高的细胞活力。细胞因子检测显示，与未暴露组相比，暴露组lps诱导的白细胞介素-1 β (IL-1 β)水平显著降低（p < 0.05）。相反，SMF暴露倾向于增加lps诱导的IL-1受体拮抗剂（IL-1Ra）和IL-6的水平。结论：我们的研究结果表明，SMF刺激通过降低NIH-3T3细胞的促炎细胞因子和增加抗炎细胞因子来抑制lps诱导的细胞毒性。
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-1 beta (IL-1 beta) 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.