Human neural stem cell-derived exosomes activate PINK1/Parkin pathway to protect against oxidative stress-induced neuronal injury in ischemic stroke DOI Creative Commons
Mengke Zhao, Jiayi Wang,

Shuaiyu Zhu

и другие.

Journal of Translational Medicine, Год журнала: 2025, Номер 23(1)

Опубликована: Апрель 5, 2025

Mitochondria play a critical role in oxidative stress (OS)-induced neuronal injury during ischemic stroke (IS), making them promising therapeutic targets. Mounting evidence underscores the extraordinary promise of exosomes derived from human neural stem cells (hNSCs) management central nervous system (CNS) diseases. Nonetheless, precise mechanisms by which these target mitochondria to ameliorate effects IS remain only partially elucidated. This study investigates protective hNSC (hNSC-Exos) on damage. Using rat model middle cerebral artery occlusion (MCAO) vivo and OS-induced HT22 vitro. Firstly, our research group independently isolated subsequently prepared hNSC-Exos. In vivo, MCAO rats were restored blood flow perfusion simulate ischemia-reperfusion injury, hNSC-Exos injected through stereotaxic injection into brain. Subsequently, evaluated, including histological studies, behavioral assessments. H2O2 was used OS environment MCAO, then its evaluated co-culturing with hNSC-Exos, immunofluorescence staining, western blotting (WB), quantitative real time PCR (qRT-PCR). process exploring specific mechanisms, we utilized RNA sequencing (RNA-seq) detect potential induction mitophagy cells. Afterwards, employed series mitochondrial function assessments autophagy related detection techniques, measuring membrane potential, reactive oxygen species (ROS) levels, transmission electron microscopy (TEM) imaging, monodansylcadaverine (MDC) mCherry-GFP-LC3B staining. addition, further investigated regulatory pathway using inhibitor mdivi-1 knocking out PTEN induced kinase 1 (PINK1) Administration significantly ameliorated brain tissue damage enhanced outcomes rats. treatment led reduction apoptosis facilitated normalization impaired neurogenesis neuroplasticity. Notably, application vitro resulted an upregulation cells, thereby remedying dysfunction. We demonstrate that activate via PINK1/Parkin pathway, improving reducing apoptosis. These findings suggest alleviate regulating pathway. reveals novel cell-derived therapy promoting neuroprotection their as approach for OS-associated CNS diseases, IS.

Язык: Английский

Role of mitophagy in mitochondrial quality control: Mechanisms and potential implications for neurodegenerative diseases DOI
Xiaole Wang, Sitong Feng, Zhen‐Zhen Wang

и другие.

Pharmacological Research, Год журнала: 2021, Номер 165, С. 105433 - 105433

Опубликована: Янв. 15, 2021

Язык: Английский

Процитировано

48
Asiatic acid alleviates ischemic myocardial injury in mice by modulating mitophagy- and glycophagy-based energy metabolism DOI Open Access
Fan Qiu, Yi Yuan, Wei Luo

и другие.

Acta Pharmacologica Sinica, Год журнала: 2021, Номер 43(6), С. 1395 - 1407

Опубликована: Сен. 14, 2021

Язык: Английский

Процитировано

43
Procyanidin A1 alleviates DSS-induced ulcerative colitis via regulating AMPK/mTOR/p70S6K-mediated autophagy DOI
Haihua Zhang, Wuying Lang, Xin Liu

и другие.

Journal of Physiology and Biochemistry, Год журнала: 2022, Номер 78(1), С. 213 - 227

Опубликована: Янв. 10, 2022

Язык: Английский

Процитировано

39
Lycorine and organ protection: Review of its potential effects and molecular mechanisms DOI
Haoxiang Xiao, Xuezeng Xu,

Luyang Du

и другие.

Phytomedicine, Год журнала: 2022, Номер 104, С. 154266 - 154266

Опубликована: Июнь 10, 2022

Язык: Английский

Процитировано

31
Human neural stem cell-derived exosomes activate PINK1/Parkin pathway to protect against oxidative stress-induced neuronal injury in ischemic stroke DOI Creative Commons
Mengke Zhao, Jiayi Wang,

Shuaiyu Zhu

и другие.

Journal of Translational Medicine, Год журнала: 2025, Номер 23(1)

Опубликована: Апрель 5, 2025

Mitochondria play a critical role in oxidative stress (OS)-induced neuronal injury during ischemic stroke (IS), making them promising therapeutic targets. Mounting evidence underscores the extraordinary promise of exosomes derived from human neural stem cells (hNSCs) management central nervous system (CNS) diseases. Nonetheless, precise mechanisms by which these target mitochondria to ameliorate effects IS remain only partially elucidated. This study investigates protective hNSC (hNSC-Exos) on damage. Using rat model middle cerebral artery occlusion (MCAO) vivo and OS-induced HT22 vitro. Firstly, our research group independently isolated subsequently prepared hNSC-Exos. In vivo, MCAO rats were restored blood flow perfusion simulate ischemia-reperfusion injury, hNSC-Exos injected through stereotaxic injection into brain. Subsequently, evaluated, including histological studies, behavioral assessments. H2O2 was used OS environment MCAO, then its evaluated co-culturing with hNSC-Exos, immunofluorescence staining, western blotting (WB), quantitative real time PCR (qRT-PCR). process exploring specific mechanisms, we utilized RNA sequencing (RNA-seq) detect potential induction mitophagy cells. Afterwards, employed series mitochondrial function assessments autophagy related detection techniques, measuring membrane potential, reactive oxygen species (ROS) levels, transmission electron microscopy (TEM) imaging, monodansylcadaverine (MDC) mCherry-GFP-LC3B staining. addition, further investigated regulatory pathway using inhibitor mdivi-1 knocking out PTEN induced kinase 1 (PINK1) Administration significantly ameliorated brain tissue damage enhanced outcomes rats. treatment led reduction apoptosis facilitated normalization impaired neurogenesis neuroplasticity. Notably, application vitro resulted an upregulation cells, thereby remedying dysfunction. We demonstrate that activate via PINK1/Parkin pathway, improving reducing apoptosis. These findings suggest alleviate regulating pathway. reveals novel cell-derived therapy promoting neuroprotection their as approach for OS-associated CNS diseases, IS.

Язык: Английский

Процитировано

1