Radioprotective effects and mechanism of HL-003 on radiation-induced salivary gland damage in mice

被引:6
|
作者
Ren, Jingming [1 ]
Huang, Rong [2 ,3 ]
Li, Yanjie [2 ,3 ]
Chen, Ruiyang [2 ,3 ]
Tian, Hongqi [1 ,4 ]
Liu, Chenlu [2 ,3 ]
机构
[1] Peking Union Med Coll & Chinese Acad Med Sci, Inst Radiat Med, Tianjin Key Lab Radiat Med & Mol Nucl Med, Tianjin 300192, Peoples R China
[2] Nankai Univ, Tianjin Stomatol Hosp, Sch Med, Dept Oral Med, Tianjin 300041, Peoples R China
[3] Tianjin Key Lab Oral & Maxillofacial Funct Recons, Tianjin 300041, Peoples R China
[4] KeChow Pharma Inc, Shanghai 201203, Peoples R China
关键词
DNA-REPAIR; RADIOTHERAPY; DYSFUNCTION; HEAD;
D O I
10.1038/s41598-022-12581-y
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Ionizing radiation (IR) can cause damage to the structure and function of salivary glands. Our research group independently synthesized the ROS scavenger, HL-003. The aim of this study was to explore the protective effects and underlying mechanisms of HL-003 on radiation-induced salivary gland injury. Salivary flow rate measurement, H&E staining, immunohistochemistry, FRAP, TUNEL, and western blotting were used to evaluate the radioprotective effect on salivary glands. The results showed that HL-003 protected the salivary secretion function by protecting the AQP-5 protein, on the salivary epithelial cell membrane, from IR damage. HL-003 reduced oxidative stress in the salivary gland by regulating the expression of ROS-related proteins NOX4, SOD2, and 8-OHdG. Furthermore, HL-003 downregulated the expression of p-p53, Bax, caspase 3, and caspase 9, and upregulated the expression of Bcl-2, suggesting that it could inhibit the activation of p53 to reduce cell apoptosis. In conclusion, HL-003 is an effective radioprotector that prevents damage of the radiation-induced salivary gland.
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页数:10
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