Neuroscience · 2026
Astrocytic NOX2 contributes to ROS-associated mitochondrial dysfunction in cerebral ischemia-reperfusion injury: modulation by electroacupuncture.
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Xie Qian-Yun, Sun Wen-Qiang, Zhao Meng-Meng, Song Qing, Zhang Ying-Ying, Zhang Hao, Zhang Yang, Liu Fang, Tang Wei, Li Meng-Xing
Аннотация
BACKGROUND: Cerebral ischemia-reperfusion injury (CIRI) causes severe neuronal damage, in which oxidative stress and mitochondrial dysfunction are major pathological events. Astrocytes are important regulators of redox homeostasis in the injured brain, yet whether astrocytic NADPH oxidase 2 (NOX2) contributes to mitochondrial impairment after ischemia remains poorly understood. Electroacupuncture (EA) has been reported to protect against ischemic brain injury, but the cellular mechanisms involved remain unclear.
METHODS: In this study, a mouse middle cerebral artery occlusion/reperfusion (MCAO/R) model was combined with astrocyte-specific NOX2 knockdown using stereotactic viral delivery. Neurological deficits, infarct size, cerebral blood flow, reactive oxygen species (ROS) accumulation, adenosine triphosphate (ATP) levels, mitochondrial morphology, and mitochondrial dynamics-associated proteins were examined.
RESULTS: MCAO/R resulted in increased astrocytic NOX2 expression, excessive ROS generation, mitochondrial fragmentation, impaired energy metabolism, and neurological dysfunction. EA treatment alleviated these changes by reducing NOX2 activation and ROS accumulation, improving mitochondrial morphology and ATP production, and restoring the balance between mitochondrial fission and fusion. These effects were reflected by decreased Drp1 and Fis1 expression and increased Mfn2 and Opa1 expression. Notably, astrocytic NOX2 knockdown produced similar protective effects and further strengthened the benefits of EA.
CONCLUSION: Astrocytic NOX2 contributes to ROS accumulation, mitochondrial dysfunction, and ischemic brain injury. EA treatment is accompanied by reduced astrocytic NOX2 expression, attenuated oxidative stress, and restoration of mitochondrial homeostasis, suggesting that regulation of astrocytic NOX2 may contribute to the protective effects of EA. Targeting astrocytic NOX2 may represent a potential therapeutic strategy for ischemic stroke.
METHODS: In this study, a mouse middle cerebral artery occlusion/reperfusion (MCAO/R) model was combined with astrocyte-specific NOX2 knockdown using stereotactic viral delivery. Neurological deficits, infarct size, cerebral blood flow, reactive oxygen species (ROS) accumulation, adenosine triphosphate (ATP) levels, mitochondrial morphology, and mitochondrial dynamics-associated proteins were examined.
RESULTS: MCAO/R resulted in increased astrocytic NOX2 expression, excessive ROS generation, mitochondrial fragmentation, impaired energy metabolism, and neurological dysfunction. EA treatment alleviated these changes by reducing NOX2 activation and ROS accumulation, improving mitochondrial morphology and ATP production, and restoring the balance between mitochondrial fission and fusion. These effects were reflected by decreased Drp1 and Fis1 expression and increased Mfn2 and Opa1 expression. Notably, astrocytic NOX2 knockdown produced similar protective effects and further strengthened the benefits of EA.
CONCLUSION: Astrocytic NOX2 contributes to ROS accumulation, mitochondrial dysfunction, and ischemic brain injury. EA treatment is accompanied by reduced astrocytic NOX2 expression, attenuated oxidative stress, and restoration of mitochondrial homeostasis, suggesting that regulation of astrocytic NOX2 may contribute to the protective effects of EA. Targeting astrocytic NOX2 may represent a potential therapeutic strategy for ischemic stroke.