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400038 重庆,陆军军医大学(第三军医大学)军事预防医学系军队劳动卫生学教研室,电磁辐射医学防护教育部重点实验室
[余争平,E-mail:yuzping_tmmu@126.com YU Zhengping, E-mail:yuzping_tmmu@126.com
收稿:2020-08-18,
修回:2020-09-28,
纸质出版:2020-12-15
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高鹏, 卢永辉, 马秦龙, 等. NLRP3炎症小体激活在太赫兹暴露所致小鼠皮肤炎症中的作用[J]. 第三军医大学学报, 2020,43(23):2290-2295.
Peng GAO, Yonghui LU, Qinlong MA, et al. NLRP3 inflammasome activation mediates terahertz exposure-induced skin aseptic inflammation in mice[J]. Journal of Third Military Medical University, 2020, 43(23): 2290-2295.
高鹏, 卢永辉, 马秦龙, 等. NLRP3炎症小体激活在太赫兹暴露所致小鼠皮肤炎症中的作用[J]. 第三军医大学学报, 2020,43(23):2290-2295. DOI: 10.16016/j.1000-5404.202008142.
Peng GAO, Yonghui LU, Qinlong MA, et al. NLRP3 inflammasome activation mediates terahertz exposure-induced skin aseptic inflammation in mice[J]. Journal of Third Military Medical University, 2020, 43(23): 2290-2295. DOI: 10.16016/j.1000-5404.202008142.
目的
2
研究太赫兹(terahertz,THz)辐射暴露对小鼠皮肤组织可能的损伤影响,探讨太赫兹暴露致皮肤无菌性炎症的潜在机制。
方法
2
采用C57BL/6J小鼠为实验动物模型,使用频率为0.22 THz的太赫兹辐射局部暴露小鼠皮肤组织,太赫兹峰值功率密度为25、80、160 mW/cm
2
,占空比1:5,暴露时间5 min和10 min。暴露后观察动物皮肤炎症因子释放、氧化应激反应和NLRP3炎症小体激活。并通过Caspase-1抑制剂,探讨NLRP3炎症小体激活在太赫兹辐射致皮肤炎症中的作用。
结果
2
160 mW/cm
2
太赫兹辐照10 min可导致小鼠皮肤氧化应激反应,并引起皮肤组织内IL-1β、IL-6和PGE2含量升高(
P
<
0.05)。80 mW/cm
2
和160 mW/cm
2
暴露10 min均可导致皮肤组织NLRP3炎症小体激活,而Caspase-1抑制剂则可显著降低皮肤组织炎症因子水平(
P
<
0.05)。
结论
2
太赫兹电磁辐射暴露能够引起小鼠皮肤氧化应激反应和无菌性炎症,NLRP3炎症小体激活则介导了太赫兹暴露所致的皮肤组织炎症,并可能与氧化应激有关。
Objective
2
To investigate the biological effects of terahertz (THz) exposure on the skin injury of mice
and explore the mechanism of the induced skin aseptic inflammation.
Methods
2
The hair-removed skin in the back of C57BL/6J mice were exposed to 0.22 THz irradiation
at a peak power density of 25
80 and 160 mW/cm
2
respectively and a duty factor of 1: 5
for 5 or 10 min. The release of inflammatory factors
oxidative stress and activation of NLR P3 inflammasome were detected after the exposure. Caspase-1 specific inhibitor Z-YVAD was employed to determine the role of the activation in the inflammation.
Results
2
Exposure to 160 mW/cm
2
THz irradiation for 10 min induced oxidative stress
and the releases of PGE2
IL-1β and IL-6 in the skin (
P
<
0.05). And the 80 mW/cm
2
and 160 mW/cm
2
THz exposure activated the NLRP3 inflammasome in the skin
and the Caspase-1 inhibitor reduced the inflammatory factors induced by the THz irradiation (
P
<
0.05).
Conclusion
2
THz exposure induces oxidative stress and aseptic inflammation. Activation of NLRP3 inflammasome mediates the skin aseptic inflammation induced by THz irradiation
which might be associated with oxidative stress.
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