| 靶向神经节巨噬细胞改善心肌梗死后心律失常 |
| 投稿时间：2024-11-01 修订日期：2024-11-17 点此下载全文 |
| 引用本文：刘恒洋,席浩淞,江洪,余锂镭.靶向神经节巨噬细胞改善心肌梗死后心律失常[J].医学研究杂志,2025,54(4):28-33 |
| DOI：
10.11969/j.issn.1673-548X.2025.04.007 |
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| 基金项目:国家自然科学基金资助项目(面上项目)(82270532)；国家自然科学基金专项项目(82241057) |
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| 中文摘要:目的 探索氯膦酸二钠脂质体消耗左侧星状神经节巨噬细胞对比格犬急性心肌梗死后室性心律失常的影响。方法 12只成年雄性比格犬,分为对照组和治疗组,对照组于左侧星状神经节(left stellate ganglion, LSG)予以注射磷酸盐缓冲盐水,而治疗组则于LSG注射氯膦酸二钠脂质体。急性心肌梗死造模后,记录心电图,测量神经功能与活性,分析心率变异性分,苏木精-伊红染色用于观察心肌细胞组织的病理变化,免疫荧光染色用于验证氯膦酸二钠脂质体对巨噬细胞的清除作用,荧光定量聚合酶链反应检测LSG中核转录因子κB(nuclear factor-kappa B, NF-κB)相关基因表达水平。结果 治疗组室性心律失常明显减少,差异有统计学意义(P＜0.05),显著抑制心肌梗死后LSG的过度激活,改善心率变异性,苏木精-伊红染色未见显著损伤,巨噬细胞显著减少,NF-κB通路相关基因表达下降(P＜0.05)。结论 氯膦酸二钠脂质体消耗LSG的巨噬细胞减轻由心肌梗死引发的心脏交感神经过度激活以及室性心律失常,其治疗效果可能通过对NF-κB信号通路的抑制起作用。 |
| 中文关键词:巨噬细胞 左侧星状神经节 氯膦酸二钠脂质体 心律失常 |
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| Targeting Ganglionic Macrophages to Improve Post-infarction Arrhythmias. |
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| Abstract:Objective Exploring the effect of clodronate liposome depletion of left stellate ganglion macrophages on ventricular arrhythmias after acute infarction in Beagle dogs. Methods Twelve adult male Beagles were divided into clod and control groups, with the Control group receiving microinjections of phosphate-buffered saline in the left stellate ganglion (LSG) and the Clod group receiving clodronate liposome. After modelling of acute cardiac infarction, electrocardiograms were recorded, neural function and activity were measured, heart rate variability scores were analysed, hematoxylin-eosin staining was used to observe pathological changes in cardiomyocyte tissues. Immunofluorescence staining was used to verify the clearance of macrophages by disodium clodronate liposomes and fluorescence quantitative polymerase chain reaction was used to detect the level of expression of nuclear factor-kappa B (NF-κB)-related genes in LSG. Results Ventricular arrhythmias were significantly reduced in the clod group, with statistically significant differences (P<0.05), significant inhibition of post-infarction LSG overactivation, improvement of heart rate variability, no significant impairment of hematoxylin-eosin staining, significant reduction in macrophages, and decreased expression of genes related to the NF-κB pathway (P<0.05). Conclusion Clodronate-liposomes improve post-infarction arrhythmias by depletion of left stellate ganglion macrophages. The therapeutic effect may be through an inhibitory effect on the NF-κB signalling pathway. |
| keywords:Macrophage Left stellate ganglion Clodronate-liposomes Arrhythmias |
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