| 褪黑素通过激活下丘脑室旁核SIRT1/炎症因子改善缺血性心力衰竭 |
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| 引用本文： | 杨金保,陈文生,张金洲,俞世强,李滨,李健,董小超. 褪黑素通过激活下丘脑室旁核SIRT1/炎症因子改善缺血性心力衰竭[J]. 心脏杂志, 2019, 31(5): 497. DOI: 10.12125/j.chj.201906024 |
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| 作者姓名： | 杨金保 陈文生 张金洲 俞世强 李滨 李健 董小超 |
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| 作者单位： | 1.西安国际医学中心心血管外科，陕西 西安 710100 |
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| 基金项目： | 国家重点研发计划项目资助（2016YFC1301900）；陕西省自然科学基金项目资助（2014JM4106） |
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| 摘 要： | 目的 探讨室旁核输注褪黑素通过激活下丘脑室旁核SIRT1信号通道并调控炎症因子改善缺血性心衰的机制。 方法 在室旁核植入微型渗透胶囊泵并输注褪黑素，1周后建立大鼠缺血性心衰模型。4周后行超声心动图监测心功能指标，采用免疫荧光法检测室旁核SIRT1活性，采用Western blot测定促炎因子IL-1β和抗炎因子IL-10的蛋白表达水平，采用ELISA试剂盒检测外周血中去甲肾上腺素（NE）的表达。 结果 室旁核输注褪黑素显著提高SIRT1活性，降低IL-1β蛋白表达水平，提高 IL-10蛋白表达水平，降低NE的表达，显著改善大鼠心脏功能。 结论 室旁核输注褪黑素改善缺血性心衰的作用是通过激活下丘脑室旁核SIRT1信号通道，调控炎症因子，并进一步降低外周交感神经活动来实现的。
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| 关 键 词： | 室旁核 褪黑素 缺血性心衰 SIRT1 炎症因子 |
| 收稿时间： | 2019-06-07 |
Melatonin Improves Ischemic Heart Failure by Activating SIRT1/Inflammatory Factors |
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| Affiliation: | 1.Department of Cardiovascular Surgery, Xi’an International Medical Center, Xi’an 710100, Shaanxi, China2.Department of Cardiovascular Surgery, Xijing Hospital, Air Force Medical University, Xi’an 710032, Shaanxi, China |
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| Abstract: | AIM To investigate the effect of melatonin infused in paraventricular nucleuses (PVN) to ameliorate ischemic heart failure and its mechanism by activating the SIRT1 signaling pathway and regulating inflammatory factors in the PVN. METHODS Osmotic mini-pumps were implanted in PVN for chronic infusion of melatonin and the rat ischemic heart failure model was established one week later. After four weeks, the indexes of echocardiography were measured, and the activity of SIRT1 and norepinephrine levels of proinflammatory factor IL-1β and anti-inflammatory factor IL-10 in the PVN were determined using Western blot and immunofluorescence. The expression of norepinephrine in peripheral blood was detected using ELISA kit. RESULTS Melatonin infusion in the PVN increased the activity of SIRT1 and protein expression level of IL-10, reduced the expression level of IL-1β and NE and improved obviously the cardiac functions in rats. CONCLUSION PVN infusion of melatonin ameliorates ischemic heart failure by activating the SIRT1 signaling pathway, regulating inflammatory factors in the paraventricular nucleuses and reducing peripheral sympathetic activity in ischemic heart failure rats. |
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