Effect of combined radiation injury on cell death and inflammation in skin.
Effect of combined radiation injury on cell death and inflammation in skin.
复制标题
联合辐射损伤对皮肤细胞死亡和炎症的影响。
DOI：
10.1007/s10495-015-1116-2
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发表时间：
2015
期刊：
影响因子：
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通讯作者：
Rodgers,KathleenE
中科院分区：
文献类型：
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作者：
Jadhav,SachinS;Meeks,ChristopherJ;Mordwinkin,NicholasM;Espinoza,TheresaB;Louie,StanG;diZerega,GereS;Rodgers,KathleenE
在发生核灾难时，离辐射源最近的个人将受到复合辐射损伤。由于辐射延迟皮肤修复，本研究的目的是阐明复合辐射和烧伤（CRBI）对皮肤损伤部位细胞凋亡和炎症的影响。将雄性C57 B1/6小鼠暴露于无损伤、仅热损伤、仅辐射（1和6戈伊）和CRBI（1和6戈伊），并在皮肤收集后的不同时间处以安乐死。TUNEL染色显示，CRBI 6戈伊组细胞凋亡反应延迟，凋亡反应增强。与其他损伤相比，这与活细胞恢复减少有关。当比较CRBI 6戈伊和热损伤之间的切割半胱天冬酶-3免疫组织化学染色时，观察到类似的反应。TNFR 1、caspase 8、Bax和IL-6 mRNA表达显示，与单纯热损伤相比，高CRBI组mRNA表达延迟增加。CRBI 6戈伊组RIPK 1 mRNA表达和坏死细胞计数延迟至第5天。CRBI 6戈伊组TNF-α和NFκB表达于第1天达高峰，明显高于其他损伤组。此外，与热损伤本身相比，CRBI 6戈伊组的炎症细胞计数在早期时间点较低。这些数据表明，CRBI延迟和加剧皮肤中的细胞凋亡和炎症，以及增加坏死，从而导致延迟的伤口愈合。
In the event of a nuclear disaster, the individuals proximal to the source of radiation will be exposed to combined radiation injury. As irradiation delays cutaneous repair, the purpose of this study was to elucidate the effect of combined radiation and burn injury (CRBI) on apoptosis and inflammation at the site of skin injury. Male C57Bl/6 mice were exposed to no injury, thermal injury only, radiation only (1 and 6 Gy) and CRBI (1 and 6 Gy) and euthanized at various times after for skin collection. TUNEL staining revealed that the CRBI 6 Gy group had a delayed and increased apoptotic response. This correlated with decreased recovery of live cells as compared to the other injuries. Similar response was observed when cleaved-caspase-3 immunohistochemical staining was compared between CRBI 6 Gy and thermal injury. TNFR1, caspase 8, Bax and IL-6 mRNA expression revealed that the higher CRBI group had delayed increase in mRNA expression as compared to thermal injury alone. RIPK1 mRNA expression and necrotic cell counts were delayed in the CRBI 6 Gy group to day 5. TNF-α and NFκB expression peaked in the CRBI 6 Gy group at day 1 and was much higher than the other injuries. Also, inflammatory cell counts in the CRBI 6 Gy group were lower at early time points as compared to thermal injury by itself. These data suggest that CRBI delays and exacerbates apoptosis and inflammation in skin as well as increases necrosis thus resulting in delayed wound healing.