Projects per year
Abstract
Background: Cerebral ischemia–reperfusion (I/R) injury is a critical pathological process in stroke, characterized by disrupted energy metabolism, inflammatory responses, and mitochondrial dysfunction. Targeting mitochondrial dynamics presents promising
strategies for alleviating brain injury. This study investigates the role and mechanism of Gastrodin (Gas) in regulating mitochondrial dynamics and mitigating cerebral I/R injury via activation of the AMPK-OPA1 signaling pathway.
Methods: An in vitro oxygen–glucose deprivation/reperfusion (OGD/R) model and an in vivo middle cerebral artery occlusion/ reperfusion (MCAO/R) model were used to assess the effects of Gas on inflammation, mitochondrial function, and energy metabolism. Immunofluorescence, western blotting (WB), reverse-transcription PCR (RT-PCR), JC-1
staining, and molecular docking techniques were employed for analysis.
Results: Gas activated the AMPK-OPA1 signaling pathway, promoting mitochondrial fusion, restoring membrane potential, enhancing ATP production, and rebalancing NAD+/NADH levels. Additionally, Gas significantly suppressed I/R-induced inflammatory responses, reduced neuronal damage, and decreased infarct volume. Notably, its protective effects on mitochondrial fusion and neuroprotection were abolished under AMPK silencing, highlighting the critical role of the AMPK-OPA1 pathway.
Conclusion: Gas alleviates cerebral I/R injury by regulating mitochondrial dynamics via the AMPK-OPA1 signaling pathway. These findings provide a theoretical basis for the therapeutic application of Gas in stroke and offer new insights into mitochondrial-targeted
treatment strategies.
strategies for alleviating brain injury. This study investigates the role and mechanism of Gastrodin (Gas) in regulating mitochondrial dynamics and mitigating cerebral I/R injury via activation of the AMPK-OPA1 signaling pathway.
Methods: An in vitro oxygen–glucose deprivation/reperfusion (OGD/R) model and an in vivo middle cerebral artery occlusion/ reperfusion (MCAO/R) model were used to assess the effects of Gas on inflammation, mitochondrial function, and energy metabolism. Immunofluorescence, western blotting (WB), reverse-transcription PCR (RT-PCR), JC-1
staining, and molecular docking techniques were employed for analysis.
Results: Gas activated the AMPK-OPA1 signaling pathway, promoting mitochondrial fusion, restoring membrane potential, enhancing ATP production, and rebalancing NAD+/NADH levels. Additionally, Gas significantly suppressed I/R-induced inflammatory responses, reduced neuronal damage, and decreased infarct volume. Notably, its protective effects on mitochondrial fusion and neuroprotection were abolished under AMPK silencing, highlighting the critical role of the AMPK-OPA1 pathway.
Conclusion: Gas alleviates cerebral I/R injury by regulating mitochondrial dynamics via the AMPK-OPA1 signaling pathway. These findings provide a theoretical basis for the therapeutic application of Gas in stroke and offer new insights into mitochondrial-targeted
treatment strategies.
| Original language | English |
|---|---|
| Journal | CNS Neuroscience and Therapeutics |
| Volume | 31 |
| Issue number | 8 |
| Publication status | Published - 2025 |
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Dive into the research topics of 'Gastrodin attenuates cerebral ischemia-reperfusion injury by enhancing mitochondrial fusion and activating the AMPK-OPA1 signaling pathway'. Together they form a unique fingerprint.Projects
- 1 Finished
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SIP High-quality Innovation Platform for chronic diseases
Fu, L. (PI), Zhang, X. (Team member), Liu, X. (Team member), Wang, R. (Team member), Li, Y. (Team member), Ruan, G. (Team member), Chen, J. (Team member), Zhang, J. (Team member), Lee, M. H. (Team member), Wang, Y. (Team member), Chen, Y. (Team member), Guo, J. (Team member), Gu, J. (Team member), Wang, Y. (Team member), Hong, M. (Team member), Yue, Y. (Team member), Guo, H. (Team member), Xu, H. (Team member), Yang, D. (Team member), Cheng, J. (Team member), Ding, D. (Team member), Zhu, W. (Team member), Cheng, K. (Team member), Huang, D. (Team member), Song, J. (Team member) & He, Y. (Team member)
1/09/22 → 30/08/26
Project: Governmental Research Project
Activities
- 1 Completed SURF Project
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Evaluation of Phenylbutyric Acid in Alcohol-Induced Mucosal Injury: Validation, Cytoprotection, and Modulation of Antioxidant Pathways
Zhang, J. (Supervisor)
6 Jul 2025 → 20 Aug 2025Activity: Supervision › Completed SURF Project
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