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极低水平的微波可减轻小鼠吸入低水平甲苯所致的免疫失衡。

Extremely low-level microwaves attenuate immune imbalance induced by inhalation exposure to low-level toluene in mice.

作者信息

Novoselova Elena G, Glushkova Olga V, Khrenov Maxim O, Novoselova Tatyana V, Lunin Sergey M, Fesenko Eugeny E

机构信息

a Department of Reception Mechanisms , Institute of Cell Biophysics , Pushchino , Moscow Region , Russia.

出版信息

Int J Radiat Biol. 2017 May;93(5):535-543. doi: 10.1080/09553002.2017.1270473. Epub 2017 Jan 9.

Abstract

PURPOSE

To clarify whether extremely low-level microwaves (MW) alone or in combination with p38 inhibitor affect immune cell responses to inhalation exposure of mice to low-level toluene.

MATERIALS AND METHODS

The cytokine profile, heat shock proteins expression, and the activity of several signal cascades, namely, NF-κB, SAPK/JNK, IRF-3, p38 MAPK, and TLR4 were measured in spleen lymphocytes of mice treated to air-delivered toluene (0.6 mg/m) or extremely low-level microwaves (8.15-18 GHz, 1μW/cm, 1 Hz swinging frequency) or combined action of these two factors.

RESULTS

A single exposure to air-delivered low-level toluene induced activation of NF-κB, SAPK/JNK, IFR-3, p38 MAPK and TLR4 pathways. Furthermore, air toluene induced the expression of Hsp72 and enhanced IL-1, IL-6, and TNF-α in blood plasma, which is indicative of a pro-inflammatory response. Exposure to MW alone also resulted in the enhancement of the plasma cytokine values (e.g. IL-6, TNF-α, and IFN-γ) and activation of the NF-κB, MAPK p38, and especially the TLR4 pathways in splenic lymphocytes. Paradoxically, pre-exposure to MW partially recovered or normalized the lymphocyte parameters in the toluene-exposed mice, while the p38 inhibitor XI additionally increased protective activity of microwaves by down regulating MAPKs (JNK and p38), IKK, as well as expression of TLR4 and Hsp90-α.

CONCLUSIONS

The results suggest that exposure to low-intensity MW at specific conditions may recover immune parameters in mice undergoing inhalation exposure to low-level toluene via mechanisms involving cellular signaling.

摘要

目的

阐明极低频微波单独作用或与p38抑制剂联合作用时,是否会影响小鼠吸入低浓度甲苯后的免疫细胞反应。

材料与方法

检测经空气吸入低浓度甲苯(0.6 mg/m)、极低频微波(8.15 - 18 GHz,1μW/cm,1 Hz摆动频率)或这两种因素联合作用处理的小鼠脾脏淋巴细胞中的细胞因子谱、热休克蛋白表达以及几种信号级联反应(即NF-κB、SAPK/JNK、IRF-3、p38 MAPK和TLR4)的活性。

结果

单次经空气吸入低浓度甲苯可诱导NF-κB、SAPK/JNK、IFR-3、p38 MAPK和TLR4信号通路的激活。此外,空气甲苯暴露可诱导Hsp72表达,并使血浆中IL-1、IL-6和TNF-α升高,这表明存在促炎反应。单独暴露于微波也会导致血浆细胞因子值升高(如IL-6、TNF-α和IFN-γ),并激活脾脏淋巴细胞中的NF-κB、p38 MAPK,尤其是TLR4信号通路。矛盾的是,预先暴露于微波可部分恢复或使甲苯暴露小鼠的淋巴细胞参数正常化,而p38抑制剂XI通过下调MAPKs(JNK和p38)、IKK以及TLR4和Hsp90-α的表达,进一步增强了微波的保护活性。

结论

结果表明,在特定条件下暴露于低强度微波,可能通过细胞信号传导机制恢复吸入低浓度甲苯小鼠的免疫参数。

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