吡咯喹啉醌在抗腮腺辐射损伤的保护作用研究
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  • 英文篇名:The protective effects of pyrroloquinoline quinone on paratid gland damage induced by irradiation
  • 作者:黄元清 ; 苗登顺 ; 陈宁
  • 英文作者:HUANG Yuanqing;MIAO Dengshun;CHEN Ning;School of Stomatology,Hunan University of Medicine;State Key Laboratory of Reproductive Medicine,The Research Center for Bone and Stem Cells,Department of Anatomy,Histology and Embryology,Nanjing Medical University;Institute of Stomatology,Nanjing Medical University;
  • 关键词:吡咯喹啉醌 ; 腮腺 ; 氧化应激 ; 全身辐射
  • 英文关键词:Pyrroloquinoline quinone;;Paratid glands;;Oxidative stress;;Total body irradiation
  • 中文刊名:SYKQ
  • 英文刊名:Journal of Practical Stomatology
  • 机构:湖南医药学院口腔医学院;南京医科大学解剖医学系骨与干细胞研究中心;南京医科大学口腔医学院;
  • 出版日期:2018-07-30
  • 出版单位:实用口腔医学杂志
  • 年:2018
  • 期:v.34;No.171
  • 基金:湖南省自然科学基金(编号:2016JJ4063);; 湖南省教育厅科学研究优秀青年项目(编号:14B141)
  • 语种:中文;
  • 页:SYKQ201804004
  • 页数:5
  • CN:04
  • ISSN:61-1062/R
  • 分类号:15-19
摘要
目的:研究吡咯喹啉醌(PQQ)通过对全身辐射(TBI)诱导的C57BL/6J小鼠腮腺损伤的保护作用。方法:随机将30只8周龄雌性C57BL/6J小鼠分成3组(n=10):未治疗组;4 Gy TBI组;4 Gy TBI加正常饮食添加PQQ组。4周后,取腮腺组织进行病理学和生化指标的测定。结果:PQQ部分纠正了TBI诱导的腮腺损伤,主要通过多个方面发挥对受损腮腺的辐射保护作用,如促细胞增殖、抑制细胞凋亡和衰老、上调抗氧化能力、清除氧自由基、减少DNA损伤。结论:PQQ可能通过上调抗氧化能力、抑制氧化应激,参与DNA损伤修复作用,从而发挥对TBI诱导腮腺损伤的辐射保护作用。
        Objective: To investigate the effects of pyrroloquinoline quinone( PQQ) on paratid gland damage induced by total body irradiation( TBI). Methods: 30 female 8-week-old C57 BL/6 J mice were randomly assigned into 3 groups( n = 10) : Untreated; 4 gray( Gy) X-ray radiation and 4 Gy X-ray radiation with additional dietary of PQQ. After 4 weeks,parotid glands tissues were collected for evaluating pathological and biochemical parameters. Results: The results indicated that PQQ partially rescued TBI induced damage of parotid glands. PQQ played radio-protective effects on parotid glands through multiple aspects,such as promoting cell proliferation,inhibiting cell apoptosis and senescence,up-regulating antioxidant ability,scavenging ROS and reducing DNA damage.Conclussion: PQQ plays a radio-protective role in parotid gland damage induced by TBI,possibly via inhibiting oxidative stress and participating in DNA damage repair.
引文
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