期刊
CHEMISTRY & BIOLOGY
卷 22, 期 2, 页码 206-216出版社
CELL PRESS
DOI: 10.1016/j.chembiol.2014.12.009
关键词
-
资金
- NIAID [AI080405]
- American Cancer Society [122059-PF-12-107-01-COD]
- Biomedical Laboratory Research and Development Service of the VA Office of Research and Development [I01BX007080]
- Van Vleet Endowment
Pharmacological mitigation of injuries caused by high-dose ionizing radiation is an unsolved medical problem. A specific nonlipid agonist of the type 2 G protein coupled receptor for lysophosphatidic acid (LPA(2)) 2-[4-(1,3-dioxo-1H, 3H-benzoisoquinolin-2-yl) butylsulfamoyl] benzoic acid (DBIBB) when administered with a postirradiation delay of up to 72 hr reduced mortality of C57BL/6 mice but not LPA2 knockout mice. DBIBB mitigated the gastrointestinal radiation syndrome, increased intestinal crypt survival and enterocyte proliferation, and reduced apoptosis. DBIBB enhanced DNA repair by augmenting the resolution of gamma-H2AX foci, increased clonogenic survival of irradiated IEC-6 cells, attenuated the radiation-induced death of human CD34(+) hematopoietic progenitors and enhanced the survival of the granulocyte/macrophage lineage. DBIBB also increased the survival of mice suffering from the hematopoietic acute radiation syndrome after total-body irradiation. DBIBB represents a drug candidate capable of mitigating acute radiation syndrome caused by high-dose gamma-radiation to the hematopoietic and gastrointestinal system.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据