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中华脑血管病杂志(电子版) ›› 2026, Vol. 20 ›› Issue (02) : 185 -196. doi: 10.3877/cma.j.issn.1673-9248.2026.02.011

基础研究

动力相关蛋白1介导线粒体裂变对缺血神经元泛凋亡的影响
王红蕊1,2, 江倩1,2, 穆长青1,2, 李响2, 耿晓坤1,2,†(), 李凤武1,2,†()   
  1. 1　101100　北京，首都医科大学附属北京潞河医院中美神经研究所
    2　101100　北京，首都医科大学附属北京潞河医院神经内科
  • 收稿日期:2025-12-22 出版日期:2026-04-01
  • 通信作者: 耿晓坤, 李凤武
  • 基金资助:
    国家自然科学基金青年项目(82501754); 北京市自然科学基金面上项目(7252075); 北京市通州区科技计划项目（课题）(WS2025031)

Dynamin-related protein 1-mediated mitochondrial fission regulates PANoptosis in ischemic neurons

Hongrui Wang1,2, Qian Jiang1,2, Changqing Mu1,2, Xiang Li2, Xiaokun Geng1,2,†(), Fengwu Li1,2,†()   

  1. 1 China‐America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing 101100, China
    2 Department of Neurology, Beijing Luhe Hospital, Capital Medical University, Beijing 101100, China
  • Received:2025-12-22 Published:2026-04-01
  • Corresponding author: Xiaokun Geng, Fengwu Li
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引用本文：

王红蕊, 江倩, 穆长青, 李响, 耿晓坤, 李凤武. 动力相关蛋白1介导线粒体裂变对缺血神经元泛凋亡的影响[J/OL]. 中华脑血管病杂志(电子版), 2026, 20(02): 185-196.

Hongrui Wang, Qian Jiang, Changqing Mu, Xiang Li, Xiaokun Geng, Fengwu Li. Dynamin-related protein 1-mediated mitochondrial fission regulates PANoptosis in ischemic neurons[J/OL]. Chinese Journal of Cerebrovascular Diseases(Electronic Edition), 2026, 20(02): 185-196.

目的

研究线粒体裂变动力相关蛋白1（Drp1）在氧葡萄糖剥夺（OGD）和再恢复（OGD/R）模型中对神经元泛凋亡的影响。

方法

体外培养SH-SY5Y细胞，建立OGD和OGD/R模型，使用CCK-8法确定Drp1抑制剂Mdivi-1的最佳干预浓度。将细胞分为对照组、OGD组、OGD/R组、OGD+Mdivi-1组、OGD/R+Mdivi-1组、OGD/R-2 h+Mdivi-1组和OGD/R-4 h+Mdivi-1组，后4组分别在OGD即刻、OGD即刻/R、OGD/R再恢复2 h后及4 h后加入Mdivi-1（10 μmol/L）处理。采用DCFH-DA和Mito-SOX法检测活性氧（ROS）水平；采用JC-1法检测线粒体膜电位；采用蛋白质印迹法检测线粒体裂变相关蛋白[磷酸化动力相关蛋白1（p-Drp1）、线粒体裂变蛋白1（Fis1）、线粒体裂变因子（Mff）]和泛凋亡相关蛋白[凋亡：B淋巴细胞瘤-2（Bcl-2）、Bcl-2相关X蛋白（Bax）、裂解的胱天蛋白酶3（cleaved caspase-3）；焦亡：NOD样受体蛋白3（NLRP3）、Gasdermin D-N端（GSDMD-N）；坏死性凋亡：受体相互作用蛋白激酶3（RIPK3）、磷酸化混合谱系激酶域样蛋白（p-MLKL）]的表达情况。2组数据比较时，若数据正态且方差齐则采用独立样本t检验，若不符合则采用非参检验（Mann-Whitney U检验）。2组以上数据差异使用单因素方差分析进行比较，并采用LSD-t检验或Dunnett's T3法进行组间两两比较。

结果

与对照组细胞相比，OGD/R与OGD损伤均能显著诱导线粒体过度裂变、导致线粒体功能障碍，并同时激活凋亡、焦亡与坏死性凋亡通路。OGD诱导的线粒体裂变及泛凋亡相关蛋白相对表达水平[GSDMD-N（2.70±0.38 vs 2.12±0.26）、p-MLKL（2.83±0.72 vs 1.76±0.20）、p-Drp1/Drp1（4.54±0.94 vs 2.53±0.47）和Mff（1.80±0.14 vs 1.37±0.10）]均显著高于OGD/R，差异均有统计学意义（t=3.761、5.049、3.821、5.181，P=0.044、0.009、0.024、0.011）。10 μmol/L的Mdivi-1能显著提高OGD[（66.79±6.54）% vs（48.60±4.66）%]、OGD/R [（76.68±6.55）% vs （59.96±5.18）% ]、OGD/R后2 h [（86.17±8.95）% vs （59.33±6.90）%]、OGD/R后4 h [（93.91±7.28）% vs （59.33±6.90）% ]的细胞存活率，差异均有统计学意义（t=4.527、3.008、4.747、6.892，P=0.025、0.030、0.016、0.001）。10 μmol/L Mdivi-1干预能有效抑制OGD/R与OGD模型下的线粒体过度裂变，并显著下调泛凋亡通路的关键蛋白表达。

结论

在OGD和OGD/R模型中，Drp1介导的线粒体过度裂变是诱导神经元泛凋亡的一个共同关键机制，抑制Drp1可显著改善线粒体功能并抑制神经元细胞泛凋亡的发生。

关键词: 缺血性脑卒中, 动力相关蛋白1, 线粒体裂变, 氧葡萄糖剥夺/再恢复损伤, 泛凋亡
Objective

To investigate the role of dynamin-related protein 1 (Drp1), a mitochondrial fission protein, on neuronal PANoptosis in oxygen-glucose deprivation (OGD) and reoxygenation (OGD/R) models.

Methods

SH-SY5Y cells were cultured in vitro, and OGD and OGD/R models were established. The optimal concentration of the Drp1 inhibitor Mdivi-1 was determined by CCK-8 assay. Cells were divided into control group, OGD group, OGD/R group, OGD+Mdivi-1 group, OGD/R+Mdivi-1 group, OGD/R-2 h+Mdivi-1 group, and OGD/R-4 h+Mdivi-1 group. Mdivi-1 (10 μmol/L) was administered at the beginning of OGD and OGD/R models, and at 2 h and 4 h after reoxygenation of OGD/R, respectively. Reactive oxygen species (ROS) were detected using DCFH-DA and Mito-SOX methods. Mitochondrial membrane potential was measured by JC-1 assay. Western blotting was used to detect the expression of mitochondrial fission-related proteins [phosphorylated dynamin-related protein 1 (p-Drp1), mitochondrial fission protein 1 (Fis1), and mitochondrial fission factor (Mff)] and PANoptosis-related proteins [apoptosis: B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), cleaved cysteinyl aspartate specific proteinase 3 (cleaved caspase-3); pyroptosis: NOD-like receptor protein 3 (NLRP3), N-terminal Gasdermin D (GSDMD-N); necroptosis: receptor-interacting protein kinase 3 (RIPK3), phosphorylated mixed lineage kinase domain-like protein (p-MLKL)]. When comparing two groups of data, the independent samples t-test was used if the data were normally distributed and had homogeneity of variance; otherwise, nonparametric test (Mann-Whitney U) was applied. Differences among more than two groups were compared using one-way ANOVA, with LSD-t or Dunnett's T3 test for pairwise comparisons.

Results

Compared with the control group, both OGD/R and OGD injuries significantly induced excessive mitochondrial fission, triggered mitochondrial dysfunction, and concurrently activated apoptotic, pyroptotic, and necroptotic pathways. The relative expression levels of mitochondrial fission and PANoptosis-related proteins induced by OGD (GSDMD-N: 2.70±0.38 vs 2.12±0.26, t=3.761, P=0.044; p-MLKL: 2.83±0.72 vs 1.76±0.20, t=5.049, P=0.009; p-Drp1/Drp1: 4.54±0.94 vs 2.53±0.47, t=3.821, P=0.024; Mff: 1.80±0.14 vs 1.37±0.10, t=5.181, P=0.011) were significantly higher than those in OGD/R. 10 μmol/L Mdivi-1 increased cell viabilities in OGD [(66.79±6.54)% vs (48.60±4.66)%, t=4.527, P=0.025], OGD/R [(76.68±6.55)% vs (59.96±5.18)%, t=3.008, P=0.030], OGD/R-2 h [(86.17±8.95)% vs (59.33±6.90)%, t=4.747, P=0.016], and OGD/R-4 h [(93.91±7.28)% vs (59.33±6.90)%, t=6.892, P=0.001] groups, with statistically significant differences. Intervention with 10 μmol/L Mdivi-1 effectively inhibited excessive mitochondrial fission in both OGD/R and OGD models, and significantly downregulated the expression of key proteins in the pathway.

Conclusion

In OGD and OGD/R models, Drp1-mediated excessive mitochondrial fission is a common critical mechanism inducing neuronal PANoptosis. Inhibiting Drp1 significantly improves mitochondrial function and suppresses the occurrence of neuronal PANoptosis.

Key words: Ischemic stroke, Dynamin-related protein 1, Mitochondrial fission, Oxygen-glucose deprivation / reoxygenation injury, PANoptosis
图1 各组细胞的存活率比较。图a为氧葡萄糖剥夺/再恢复（OGD/R）模型细胞的存活率比较，使用One-way ANOVA和LSD-t检验；图b为氧葡萄糖剥夺（OGD）模型细胞的存活率比较，使用One-way ANOVA和Dunnett's T3法；图c为延迟给药细胞的存活率比较，使用One-way ANOVA和Dunnett's T3 注：OGD/R+Mdivi-1为氧葡萄糖剥夺/再恢复模型+Mdivi-1处理组；OGD+Mdivi-1为氧葡萄糖剥夺模型+Mdivi-1处理组；OGD/R-2 h+Mdivi-1为氧葡萄糖剥夺/再恢复模型+Mdivi-1延迟2 h给药组；OGD/R-4 h+Mdivi-1为氧葡萄糖剥夺/再恢复模型+Mdivi-1延迟4 h给药组
图2 氧葡萄糖剥夺（OGD）和氧葡萄糖剥夺/再恢复（OGD/R）诱导SH-SY5Y细胞泛凋亡发生的相关检测结果。图a为各组细胞凋亡相关蛋白的表达水平及定量分析；图b为各组细胞焦亡相关蛋白的表达水平及定量分析；图c为各组细胞坏死性凋亡相关蛋白的表达水平及定量分析。磷酸化混合谱系激酶域样蛋白（p-MLKL）组间比较使用One-way ANOVA和Dunnett's T3法，其余蛋白比较均使用One-way ANOVA和LSD-t检验 注：Bcl-2为B淋巴细胞瘤-2；β-Actin为β-肌动蛋白；Bax为Bcl-2相关X蛋白；Cleaved Casp-3为裂解的胱天蛋白酶3；NLRP3为NOD样受体蛋白3；GSDMD-N为Gasdermin D-N端；RIPK3为受体相互作用蛋白激酶3
图3 Mdivi-1对氧葡萄糖剥夺（OGD）和氧葡萄糖剥夺/再恢复（OGD/R）诱导的细胞泛凋亡的影响。图a为各组细胞凋亡相关蛋白的表达水平及定量分析；图b为各组细胞焦亡相关蛋白的表达水平及定量分析；图c各组细胞坏死性凋亡相关蛋白的表达水平及定量分析。OGD组的B淋巴细胞瘤-2（Bcl-2）和磷酸化混合谱系激酶域样蛋白（p-MLKL）及OGD/R组的Bcl-2相关X蛋白（Bax）和受体相互作用蛋白激酶3（RIPK3）组间比较使用Mann-Whitney U检验，其余均使用独立样本t检验 注：OGD/R+Mdivi-1为OGD/R模型+Mdivi-1处理组；OGD+Mdivi-1为OGD模型+Mdivi-1处理组；Cleaved Casp-3为裂解的胱天蛋白酶3；β-Actin为β-肌动蛋白；NLRP3为NOD样受体蛋白3；GSDMD-N为Gasdermin D-N端
图4 氧葡萄糖剥夺（OGD）和氧葡萄糖剥夺/再恢复（OGD/R）诱导SH-SY5Y细胞发生线粒体裂变的相关检测结果。组间比较均使用One-way ANOVA和LSD-t检验 注：Drp1为动力相关蛋白1；β-Actin为β-肌动蛋白；p-Drp1为磷酸化动力相关蛋白1；Fis1为线粒体裂变蛋白1；Mff为线粒体裂变因子
图5 Mdivi-1对氧葡萄糖剥夺（OGD）和氧葡萄糖剥夺/再恢复（OGD/R）诱导的SH-SY5Y细胞线粒体裂变蛋白表达的影响。组间比较均使用独立样本t检验 注：OGD/R+Mdivi-1为OGD/R模型+Mdivi-1处理组；OGD+Mdivi-1为OGD模型+Mdivi-1处理组；Drp1为动力相关蛋白；p-Drp1为磷酸化动力相关蛋白1；Fis1为线粒体裂变蛋白1；Mff为线粒体裂变因子；β-Actin为β-肌动蛋白1
图6 氧葡萄糖剥夺（OGD）和氧葡萄糖剥夺/再恢复（OGD/R）诱导SH-SY5Y细胞的线粒体功能结果。图a为各组细胞的膜电位比较；图b为线粒体活性氧（ROS）水平比较；图c为ROS代表性图像。DAPI为细胞核染色图；Merge为细胞核染色和DCFH-DA染色合并图。图a和图b均使用One-way ANOVA和LSD-t检验
图7 Mdivi-1对氧葡萄糖剥夺（OGD）和氧葡萄糖剥夺/再恢复（OGD/R）诱导SH-SY5Y细胞的线粒体功能障碍的影响。图a为各组细胞的膜电位比较；图b线粒体活性氧（ROS）水平比较；图c为ROS代表性图像。DAPI为细胞核染色图；Merge为细胞核染色和DCFH-DA染色合并图。图a和图b均使用独立样本t检验 注：OGD/R+Mdivi-1为OGD/R模型+Mdivi-1处理组；OGD+Mdivi-1为OGD模型+Mdivi-1处理组
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