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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >IL-1β is an essential mediator of the antineurogenic and anhedonic effects of stress
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IL-1β is an essential mediator of the antineurogenic and anhedonic effects of stress

机译：IL-1β是压力的抗肿瘤和无痛作用的重要介质

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摘要

Stress decreases neurogenesis in the adult hippocampus, and blockade of this effect is required for the actions of antidepressants in behavioral models of depression. However, the mechanisms underlying these effects of stress have not been identified. Here, we demonstrate an essential role for the proinf lammatory cytokine IL-1β. Administration of IL-1β or acute stress suppressed hippocam-pal cell proliferation. Blockade of the IL-1β receptor, IL-1RI, by using either an inhibitor or IL-1RI null mice blocks the antineurogenic effect of stress and blocks the anhedonic behavior caused by chronic stress exposure. In vivo and in vitro studies demonstrate that hippocampal neural progenitor cells express IL-1RI and that activation of this receptor decreases cell proliferation via the nuclear factor-κB signaling pathway. These findings demonstrate that IL-1β is a critical mediator of the antineurogenic and depres-sive-like behavior caused by acute and chronic stress.
机译：应激会降低成年海马的神经发生，因此在抑郁行为模型中抗抑郁药的作用需要阻断这种作用。但是，尚未确定这些压力作用的潜在机制。在这里，我们证明了促炎性细胞因子IL-1β的重要作用。 IL-1β或急性应激的给药抑制了河豚摄像细胞的增殖。通过使用抑制剂或IL-1RI无效小鼠对IL-1β受体IL-1RI的阻断可阻断应激的抗肿瘤作用，并阻断由慢性应激暴露引起的无性行为。体内和体外研究表明，海马神经祖细胞表达IL-1RI，并且该受体的激活通过核因子-κB信号通路降低了细胞增殖。这些发现表明，IL-1β是急性和慢性应激引起的抗肿瘤和抑郁样行为的关键介质。

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