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首页> 外文期刊>Auris, nasus, larynx >Geranylgeranylacetone suppresses noise-induced expression of proinflammatory cytokines in the cochlea
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Geranylgeranylacetone suppresses noise-induced expression of proinflammatory cytokines in the cochlea

机译：Geranylgeranylacetone抑制噪音诱导的耳蜗促炎细胞因子的表达

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Objective: Heat shock transcription factor 1 (HSF1) is a master regulator of heat shock response, and also inhibits expression of inflammatory cytokines directly or indirectly. Here, we examined effects of HSF1 activation on the expression of proinflammatory cytokines in mouse cochlea after exposure to noise. Methods: Male CBA/N mice with normal Preyer's reflex were exposed to intense noise for 3. h. Three hours after noise exposure, bilateral cochleae were removed and expression of major inflammatory cytokines was examined. Results: We found that interleukin-6 (IL-6) and interleukin-1β (IL-1β) expression increased significantly after noise exposure, and the expression was suppressed significantly in mice administered with geranylgeranylacetone (GGA), which activates HSF1. Seven days after noise exposure, thresholds for auditory brainstem response were elevated, and GGA administration significantly suppressed this elevation. Conclusion: These results suggest that HSF1-mediated suppression of proinflammatory cytokines in the cochlea by GGA administration could be an important means of inner ear protection.
机译：目的：热休克转录因子1（HSF1）是热休克反应的主要调节剂，还可以直接或间接抑制炎症细胞因子的表达。在这里，我们检查了HSF1激活对暴露于噪音后的小鼠耳蜗促炎细胞因子表达的影响。方法：将具有正常Preyer反射能力的雄性CBA / N小鼠暴露于强烈噪音下3小时。噪声暴露三小时后，去除双侧耳蜗，并检查主要炎症细胞因子的表达。结果：我们发现，噪声暴露后，白细胞介素6（IL-6）和白细胞介素1β（IL-1β）的表达显着增加，并且在施用可激活HSF1的香叶基香叶基丙酮（GGA）的小鼠中，表达被显着抑制。噪声暴露后7天，听觉脑干反应的阈值升高，GGA给药显着抑制了这种升高。结论：这些结果表明，GGA给药可抑制HSF1介导的耳蜗促炎性细胞因子，这可能是保护内耳的重要手段。

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