首页|基于NLRP3研究放射对小鼠涎腺组织损伤的影响

基于NLRP3研究放射对小鼠涎腺组织损伤的影响

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目的 研究放射对小鼠涎腺组织形态、功能及NLRP3表达的影响,为修复放射性涎腺组织损伤提供新思路。方法 建立小鼠下颌下腺放射损伤模型,记录饮水情况,于照射后1、3、7、14 d进行唾液流率检测,HE染色观察下颌下腺损伤情况,免疫组织化学法及Real-time PCR检测NLRP3及Caspase-1在小鼠放射性下颌下腺损伤中的表达情况。结果 随着时间的累积,放射组小鼠饮水量逐渐增多,唾液流率减少,下颌下腺中炎症细胞不断增多,腺泡细胞逐渐出现核固缩及空泡化等病变;在照射后的7和14 d,放射组NLRP3和Caspase-1蛋白及基因表达水平均明显高于正常组(P<0。05)。结论 辐射可诱导小鼠下颌下腺组织损伤,并激活NLRP3炎症体促使其表达量增加。
Effect of radiation on damage of mouse salivary gland tissue based on NLRP3
Objective To study the effects of radiation on the morphology,function,and NLRP3 expression of mouse salivary gland tissue,and provide new ideas to repair radiation-induced damage to salivary gland tissue.Methods We established a mouse model of radiation-induced submandibular gland injury and Recorded the weight of drinking water.The salivary flow rate was assessed,and HE staining was used to observe submandibular gland injury.Immunohistochemistry and Real-time PCR were used to assess expression of NLRP3 and Caspase-1 in the radiation-injured submandibular gland of mice at 1,3,7 and 14 days after radiation exposure.Results Over time,the amount of water consumed by radiation group mice was gradually increased,the salivary flow rate was decreased,and inflammatory cells in the submandibular gland continued to increase.Acinar cells gradually showed lesions,such as nuclear pyknosis and vacuolization.At 7 and 14 days after radiation exposure,expression levels of NLRP3 and Caspase-1 proteins and genes in the radiation group were significantly higher than those in the normal group(P<0.05).Conclusions Radiation damages mouse submandibular gland tissue and activates the NLRP3 inflammasome to increase its expression level.

NLRP3 inflammasomeradiationsalivary gland injury

吴玉琪、黄桂林、肖丽君、张敏、张霓霓

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遵义医科大学附属口腔医院,贵州遵义 563000

邵阳市中心医院口腔科,湖南邵阳 422000

遵义医科大学第五附属医院,广东珠海 519000

NLRP3炎症体 放射 涎腺损伤

国家自然科学基金国家自然科学基金遵义医科大学"未来临床名医"项目贵州省临床重点建设项目贵州省科技计划

819602048186019820211017黔卫计办涵[2017]24号黔科合基础-ZK[2024]一般339

2024

中国比较医学杂志
中国实验动物学会,中国医学科学院医学实验动物研究所

中国比较医学杂志

CSTPCD北大核心
影响因子:0.473
ISSN:1671-7856
年,卷(期):2024.34(5)