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Curr Top Med Chem. 2017;17(26):2935-2956. doi: 10.2174/1568026617666170821124947.
3
Hematological profile of untreated or ionizing radiation-exposed cyclooxygenase-2-deficient mice.未治疗或暴露于电离辐射的环氧化酶-2缺陷小鼠的血液学特征
Physiol Res. 2017 Sep 22;66(4):673-676. doi: 10.33549/physiolres.933568. Epub 2017 Apr 12.
4
Radiation triggering immune response and inflammation.辐射引发免疫反应和炎症。
Cancer Lett. 2015 Nov 28;368(2):156-63. doi: 10.1016/j.canlet.2015.04.016. Epub 2015 Apr 21.
5
Cyclooxygenase inhibitors: From pharmacology to clinical read-outs.环氧化酶抑制剂：从药理学到临床结果
Biochim Biophys Acta. 2015 Apr;1851(4):422-32. doi: 10.1016/j.bbalip.2014.09.016. Epub 2014 Sep 28.
6
Agonist of the adenosine A3 receptor, IB-MECA, and inhibitor of cyclooxygenase-2, meloxicam, given alone or in a combination early after total body irradiation enhance survival of γ-irradiated mice.腺苷 A3 受体激动剂 IB - MECA 和环氧化酶 - 2 抑制剂美洛昔康，单独使用或在全身照射后早期联合使用，均可提高受 γ 射线照射小鼠的存活率。
Radiat Environ Biophys. 2014 Mar;53(1):211-5. doi: 10.1007/s00411-013-0500-y. Epub 2013 Nov 22.
7
A single dose of an inhibitor of cyclooxygenase 2, meloxicam, administered shortly after irradiation increases survival of lethally irradiated mice.单次给予环氧化酶 2 抑制剂美洛昔康，在辐照后不久给予，可提高致死性辐照小鼠的存活率。
Radiat Res. 2011 Aug;176(2):269-72. doi: 10.1667/rr2614.1. Epub 2011 Jun 10.
8
Inhibition of cyclooxygenase 2 in mice increases production of g-csf and induces radioprotection.抑制小鼠体内的环氧化酶2可增加粒细胞集落刺激因子的产生并诱导辐射防护。
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9
The coxibs, selective inhibitors of cyclooxygenase-2.昔布类药物，即环氧化酶-2的选择性抑制剂。
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10
Prostaglandin synthase 2 gene disruption causes severe renal pathology in the mouse.前列腺素合成酶2基因破坏导致小鼠出现严重的肾脏病变。
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环氧化酶-2缺陷小鼠照射后存活受损。

Impaired post-irradiation survival of cyclooxygenase-2-deficient mice.

作者信息

Hofer M, Hoferová Z, Gruzdev A, Dušek L, Falk M

机构信息

Department of Cell Biology and Radiobiology, Institute of Biophysics of the Czech Academy of Sciences, Brno, Czech Republic.

出版信息

Physiol Res. 2018 Nov 14;67(5):809-812. doi: 10.33549/physiolres.933890. Epub 2018 Jul 25.

DOI:10.33549/physiolres.933890
PMID:30044110
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7385709/
Abstract

We investigated and evaluated post-irradiation survival in cyclooxygenase-2-deficient (COX-2 KO) mice. Thirty-day survival following exposure of COX-2 KO mice to a lethal dose of 8.5 Gy of gamma-rays was observed to be statistically significantly lower in both males and females, as well as when the sexes were merged, in comparisons with their wild-type counterparts. These findings were related to the previous observations concerning the detrimental influence of the COX-2 genetic disruption on hematopoiesis in sublethally irradiated mice. Deteriorated post-irradiation survival of COX-2 KO mice confirmed the previously anticipated conclusion regarding negative influence of the antiinflammatory action of COX-2 deficiency under the conditions of exposure of the animals to ionizing radiation.

摘要

我们研究并评估了环氧合酶-2缺陷（COX-2 KO）小鼠的辐射后存活率。与野生型对照小鼠相比，观察到COX-2 KO小鼠暴露于8.5 Gy致死剂量的γ射线后30天的存活率，在雄性和雌性小鼠中以及合并两性数据时，在统计学上均显著降低。这些发现与先前关于COX-2基因破坏对亚致死剂量辐射小鼠造血功能产生有害影响的观察结果相关。COX-2 KO小鼠辐射后存活率的恶化证实了先前预期的结论，即在动物暴露于电离辐射的条件下，COX-2缺乏的抗炎作用具有负面影响。