Abstract：
This study offers a review of published data on DNA double strand break (DSB) repair kinetics after exposure to ionizing radiation. By compiling a database, which currently includes 285 DNA DSB repair experiments utilizing both photons and ions, we investigate the impact of distinct experimental parameters on the kinetics of DNA DSB repair. Methodological differences and inconsistencies in reporting make the comparison of data generated by different research groups challenging. Nevertheless, by implementing filtering criteria, we can compare repair kinetics obtained with normal and tumor cells derived from human or animal tissues, as well as cells exposed to photons or ions ranging from hydrogen to iron ions. In addition, several repair curves of repair deficient cell lines were included. The study aims to provide researchers with a comprehensive overview of experimental factors that may confound results and emphasize the importance of precise reporting of experimental parameters. Moreover, we identify gaps in the literature that require attention in future studies, aiming to address clinically relevant questions related to radiotherapy. The database can be freely accessed at: https://github.com/weradstake/DRDNA.
摘要：
放射性肠损伤（RIID）是腹部盆腔恶性肿瘤患者放疗的常见副作用。间隙连接是由连接蛋白(Cxs)组成的特殊结构。本研究旨在探讨连接蛋白在RIID中的表达和作用及其机制。在这项研究中,用钙黄绿素-AM荧光探针检测肠上皮IEC-6细胞间隙连接细胞间通讯的变化.我们的结果表明，在照射后6、12、24和48小时，IEC-6细胞的间隙连接细胞间通讯减少，免疫印迹和免疫荧光结果显示，Cx43的表达，而不是其他连接蛋白，在辐照的肠上皮细胞中减少。Cx43的沉默降低了ROS和细胞内Ca2+水平增加的经照射的肠上皮细胞之间的间隙连接细胞间通讯。此外，敲除Cx43减少了克隆簇的数量，细胞增殖减少，细胞毒性和凋亡增加。Western印迹结果显示,Cx43的沉默导致照射的肠上皮细胞中γ-H2AX和PI3K/AKT通路蛋白的改变。PI3K/AKT途径抑制剂LY294002的施用抑制了Cx43过表达的肠上皮细胞中的辐射防护作用。我们的研究表明，Cx43表达被电离辐射降低，有利于肠上皮细胞的辐射防护。
