地方性砷中毒致病致癌机制不明，至今无特效治疗药物是限制其防治的瓶颈问题，也是各国政府和学者高度关注的重大公共卫生问题。砷暴露通过抑制DNA损伤修复基因的表达，促进砷中毒的发生发展，但机制尚不明确。新近研究表明，组蛋白H3K9me2可能在砷致DNA损伤修复过程中扮演着重要角色。本项目在课题组前期研究的基础上，从人群和细胞两个实验体系，采用酶联免疫吸附实验（ELISA）、实时荧光定量PCR（qRT-PCR）、免疫印迹(Western Blotting)、定量染色质免疫沉淀（ChIP-qPCR）等技术，同时采用组蛋白甲基化酶抑制剂、siRNA、高表达质粒和银杏制剂等处理不同体系研究对象，从正向和反向较深入系统地探讨H3K9me2在砷致DNA损伤修复中的调控机制，为地砷病的针对性预防和靶向治疗提供新思路和科学依据。

Currently, it is a bottleneck problem that the pathogenesis and carcinogenic mechanisms of endemic arsenic poisoning is unclear, and no special treatment drugs, which limit the prevention and control of endemic arsenic poisoning. Endemic arsenic poisoning is also a major public health issue that governments and scholars are highly concerned about. It has been reported that arsenic exposure can promote the development of arsenic poisoning by inhibiting the expression of DNA repair genes, but the mechanism is not clear. Recent studies have shown that H3K9me2 may play an important role in arsenic-induced DNA damage repair. In this study, based on the previous study of our research group, from research in population to the cellular level, enzyme-linked immunosorbent assay (ELISA), real-time quantitative PCR (qRT-PCR), Western Blotting, quantitative chromatin immunoprecipitation and other techniques were used. At the same time, histone methylase inhibitors, siRNA, high expression plasmids and ginkgo preparations were used to deal the subjects of different system. The aim of this study is to systematically explore the regulation mechanism of H3K9me2 in arsenic-induced DNA damage repair from both forward and reverse angles, and to provide new ideas and scientific basis for the pertinence prevention and targeted therapy of endemic arsenic poisoning.