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首页> 外文期刊>BioResearch open access. >X-Ray-Induced Damage to the Submandibular Salivary Glands in Mice: An Analysis of Strain-Specific Responses
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X-Ray-Induced Damage to the Submandibular Salivary Glands in Mice: An Analysis of Strain-Specific Responses

机译：X射线诱导小鼠下颌唾液腺的损害：应变特定反应的分析。

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Radiation therapy for head and neck cancers often causes xerostomia (dry mouth) by acutely damaging the salivary glands through the induction of severe acute inflammation. By contrast, the mechanism underlying the X-ray-induced delayed salivary dysfunction is unknown and has attracted increasing attention. To identify and develop a mouse model that distinguishes the delayed from the acute effects, we examined three different mouse strains (C57BL/6, ICR, and ICR-nuu) that showed distinct T-cell activities to comparatively analyze their responses to X-ray irradiation. Three strains were irradiated with X-rays (25 Gy), and functional changes of the submandibular glands were examined by determining pilocarpine-induced saliva secretion. Structural changes were evaluated using histopathological and immunohistochemical examinations of CD3, cleaved poly (ADP-ribose) polymerase (PARP), and Bcl-xL. In C57BL/6 mice, the X-ray irradiation induced acute inflammation accompanied by severe inflammatory cell infiltration at 4 days postirradiation, causing substantial destruction and significant dysfunction at 2 weeks. Fibrotic repair was observed at 16 weeks. In ICR-nuu mice, the inflammation and organ destruction were much milder than in the other mice strains, but increased apoptotic cells and a significant reduction in salivary secretion were observed at 4 and 8 weeks and beyond, respectively. These results suggest that in C57BL/6 mice, X-ray-induced functional and structural damage to the salivary glands is caused mainly by acute inflammation. By contrast, although neither acute inflammation nor organ destruction was observed in ICR-nuu mice, apoptotic cell death preceded the dysfunction in salivary secretion in the later phase. These data suggest that the X-ray-irradiated ICR-nuu mouse may be a useful animal model for developing more specific therapeutic methods for the delayed dysfunction of salivary glands.
机译：头颈癌的放射疗法通常通过诱发严重的急性发炎而严重损伤唾液腺，从而引起口干症（口干）。相比之下，X射线诱发的延迟唾液功能障碍的机制尚不清楚，并且引起了越来越多的关注。为了鉴定和建立区分延迟效应和急性效应的小鼠模型，我们检查了三种不同的小鼠品系（C57BL / 6，ICR和ICR-nu / nu），它们显示出不同的T细胞活性，以比较分析其对X的反应射线照射。用X射线（25 Gy）照射3个菌株，并通过测定毛果芸香碱诱导的唾液分泌来检查下颌下腺的功能变化。使用CD3，裂解的多聚（ADP-核糖）聚合酶（PARP）和Bcl-xL的组织病理学和免疫组织化学检查评估结构变化。在C57BL / 6小鼠中，X射线辐射在照射后4天引起急性炎症并伴有严重的炎症细胞浸润，从而在2周时造成实质性破坏和严重功能障碍。在第16周观察到纤维化修复。在ICR-nu / nu小鼠中，炎症和器官破坏比其他小鼠品系要轻得多，但分别在4周和8周及以后观察到凋亡细胞增加和唾液分泌显着减少。这些结果表明，在C57BL / 6小鼠中，X射线诱导的唾液腺功能和结构损伤主要是由急性炎症引起的。相比之下，尽管在ICR-nu / nu小鼠中既未观察到急性炎症也未观察到器官破坏，但在随后的阶段，凋亡的细胞死亡先于唾液分泌功能障碍。这些数据表明，X射线照射的ICR-nu / nu小鼠可能是有用的动物模型，可用于开发针对唾液腺功能障碍的更具体治疗方法。

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