| 微小RNA-10b对脓毒症急性肺损伤患者巨噬细胞胞葬的调控 |
| 投稿时间：2025-07-23 修订日期：2025-09-12 点此下载全文 |
| 引用本文：孔祥旭,苏盛元,张月辉,曲婷婷.微小RNA-10b对脓毒症急性肺损伤患者巨噬细胞胞葬的调控[J].医学研究杂志,2026,55(1):83-87, 94 |
| DOI：
10.11969/j.issn.1673-548X.2026.01.015 |
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| 基金项目:广东省深圳市科研计划项目(JCYJ20210324111013036)；广东省深圳市宝安区2024年度区属公立医院高质量发展研究项目(BAGZL2024045)；广东省深圳市宝安区医学会医疗卫生科研项目(BAYXH2023024) |
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| 中文摘要:目的 探讨微小RNA-10b(microRNA-10,miR-10b)对脓毒症急性肺损伤(acute lung injury,ALI)患者巨噬细胞胞葬的调控。方法 回顾性分析2022年10月~2024年9月在深圳市宝安区人民医院诊治的脓毒症患者130例,按是否发生ALI分为对照组(n=75)和ALI组(n=55)。比较两组miR-10b、Krüppel样因子4/Mer原癌基因酪氨酸激酶(Krüppel-like factor 4/Mer proto-oncogene tyrosine kinase,KLF4/MerTK)表达、胞葬功能,分析miR-10b表达与KLF4/MerTK、胞葬功能、ALI指标的相关性,分析miR-10b、KLF4/MerTK、胞葬功能与脓毒症ALI的联系；体外研究调控机制。结果 ALI组miR-10b表达、急性生理与慢性健康状况评估Ⅱ(acute physiology and chronic health evaluation Ⅱ,APACHE Ⅱ)评分和肿瘤坏死因子(tumor necrosis factor,TNF) -α、白细胞介素(interleukin,IL)-6水平高于对照组,KLF4、MerTK表达、胞葬功能、氧合指数(oxygenation index,OI)、IL-10水平低于对照组(P＜0.05)；miR-10b表达与KLF4/MerTK信号通路、胞葬功能、OI、IL-10水平呈负相关,与APACHE Ⅱ评分、TNF-α、IL-6水平呈正相关(P＜0.05)；miR-10b、KLF4、MerTK均是脓毒症ALI患者巨噬细胞胞葬功能缺陷的独立影响因素(P＜0.05)。体外研究显示,siKLF4细胞组KLF4、MerTK表达和胞葬功能均低于siNC细胞组(P＜0.05)。结论 miR-10b可减弱脓毒症ALI患者巨噬细胞胞葬,其机制可能与抑制KLF4/MerTK信号通路的激活有关。 |
| 中文关键词:脓毒症 急性肺损伤 微小RNA-10b KLF4/MerTK信号通路 巨噬细胞 胞葬 |
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| MicroRNA-10b Regulates Macrophage Efferocytosis in Patients with Sepsis-induced Lung Injury. |
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| Abstract:Objective To investigate the regulatory effect of microRNA-10b (miR-10b) on macrophage efferocytosis in patients with seis-induced acute lung injury (ALI). Methods A retrospective analysis was conducted on 130sepsis patients treated in Shenzhen Baoan People′s Hospital from October 2022 to September 2024. The patients were divided into control group (75 cases) and ALI group (55 cases) according to whether ALI occurred or not. The expressions of miR-10b, Krüppel-like factor 4/Mer proto-oncogene tyrosine kinase (KLF4/MerTK), and efferocytosis function were compared between the two groups; the correlation between miR-10b expression and KLF4/MerTK, efferocytosis function, and ALI indicators was analyzed; the correlation between miR-10b, KLF4/MerTK, efferocytosis and sepsis-ALI was analyze; and regulatory mechanisms was studied in vitro. Results The expression of miR-10b, APACHE Ⅱ score, and the levels of TNF-α and IL-6 in the ALI group were higher than those in the control group, and the expressions of KLF4 and MerTK, efferocytosis function, oxygenation index (OI), and IL-10 levels were lower than those in the control group (P<0.05); miR-10b expression was negatively correlated with the KLF4/MerTK signaling pathway, efferocytosis function, OI, and IL-10 levels, and positively correlated with the APACHE Ⅱ score, TNF-α, and IL-6 levels (P<0.05). miR-10b, KLF4, and MerTK were independent factors influencing the defective macrophage efferocytosis function in patients with sepsis-induced ALI (P<0.05). In vitro studies showed that the expressions of KLF4 and MerTK, and efferocytosis function in the siKLF4 cell group were lower than those in the siNC cell group (P<0.05). Conclusion miR-10b could weaken macrophage efferocytosis in patients with sepsis-induced ALI, and its mechanism may be related to the inhibition of the KLF4/MerTK signaling pathway activation. |
| keywords:Sepsis Acute lung injury MicroRNA-10b KLF4/MerTK signaling pathway Macrophage Efferocytosis |
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