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老年小鼠中血管加压素信号抑制可降低长期时差反应下的死亡率。

Vasopressin Signal Inhibition in Aged Mice Decreases Mortality under Chronic Jet Lag.

作者信息

Yamaguchi Yoshiaki, Okamura Hitoshi

机构信息

Department of Systems Biology, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan.

Department of Systems Biology, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan.

出版信息

iScience. 2018 Jul 27;5:118-122. doi: 10.1016/j.isci.2018.06.008. Epub 2018 Jul 18.

DOI:10.1016/j.isci.2018.06.008
PMID:30240642
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6123867/
Abstract

Chronic jet lag, a model of shiftwork, increases mortality in aged mice. One potential reason for this association is that the chronic desynchronization between the internal clock phase and the environmental light/dark (LD) cycle might increase the mortality rate. However, this hypothesis has not been examined because of the lack of an appropriate animal model to prove this speculation. Here, we found that rapidly entrainable vasopressin receptor V1aV1b mice showed lower mortality under a chronic jet lag condition. Moreover, we found that pharmacological inactivation of V1a and V1b signaling decreased mortality even in aged wild-type mice, thus providing a potential pharmaceutical intervention for shiftwork-related health problems.

摘要

慢性时差反应作为一种轮班工作模型,会增加老年小鼠的死亡率。这种关联的一个潜在原因是,内部时钟相位与环境光/暗(LD)周期之间的长期不同步可能会增加死亡率。然而,由于缺乏合适的动物模型来证实这一推测,该假设尚未得到验证。在此,我们发现,快速可同步的血管加压素受体V1aV1b小鼠在慢性时差反应条件下死亡率较低。此外,我们发现,即使在老年野生型小鼠中,V1a和V1b信号的药理学失活也能降低死亡率,从而为与轮班工作相关的健康问题提供了一种潜在的药物干预措施。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0658/6123867/ca1d5eac891f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0658/6123867/d34958f6a65a/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0658/6123867/30fc52563844/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0658/6123867/ca1d5eac891f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0658/6123867/d34958f6a65a/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0658/6123867/30fc52563844/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0658/6123867/ca1d5eac891f/gr2.jpg

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