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PEG300 Protects Mitochondrial Function By Upregulating PGC-1α to Delay Central Nervous System Oxygen Toxicity in Mice
1Department of Pharmacy, The First Affiliated Hospital (Changhai Hospital), Naval Medical University, Shanghai, China.
Abstract:
Central nervous system oxygen toxicity (CNS-OT) is a complication of hyperbaric oxygen (HBO) treatment, with limited prevention and treatment options available. In this study, we aimed to explore the effect of polyethylene glycol 300 (PEG300) on CNS-OT and underlying mechanisms. Motor and cognitive functions of mice in normobaric conditions were evaluated by Morris water maze, passive active avoidance, and rotarod tests. HBO was applied at 6 atmospheres absolute (ATA) for 30 min after drug administration. The latency period of convulsion in mice was recorded, and hippocampal tissues were extracted for biochemical experiments. Our experimental results showed that PEG300 extended the convulsion latencies in CNS-OT mice, reduced oxidative stress and inflammation levels in hippocampal tissues. Furthermore, PEG300 preserved mitochondrial integrity and maintained mitochondrial membrane potential in hippocampal tissue by upregulating Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha (PGC-1α). This protective effect was enhanced following the administration of ZLN005, an agonist of PGC-1a. Hence, our study suggests that PEG300 might exert protective effects by upregulating PGC-1α expression and preserving mitochondrial health, offering promising prospects for CNS-OT treatment.
Insights
Polyethylene glycol 300 (PEG300) shows promise in preventing central nervous system oxygen toxicity (CNS-OT) by reducing oxidative stress and inflammation. This compound protects brain cells and mitochondria, potentially offering a new treatment for CNS-OT.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Central nervous system oxygen toxicity (CNS-OT) is a serious complication of hyperbaric oxygen (HBO) therapy.
- Current prevention and treatment strategies for CNS-OT are limited, necessitating novel therapeutic approaches.
Purpose of the Study:
- To investigate the protective effects of polyethylene glycol 300 (PEG300) against CNS-OT in a mouse model.
- To elucidate the underlying mechanisms, particularly the role of mitochondrial function and PGC-1α.
Main Methods:
- Mice were administered PEG300 before hyperbaric oxygen (HBO) exposure at 6 ATA for 30 minutes.
- Neurological function was assessed using behavioral tests (Morris water maze, passive active avoidance, rotarod).
- Hippocampal tissues were analyzed for oxidative stress, inflammation, mitochondrial integrity, and PGC-1α expression.
Main Results:
- PEG300 significantly extended the latency to convulsions in CNS-OT mice.
- PEG300 treatment reduced oxidative stress and inflammation markers in hippocampal tissues.
- PEG300 upregulated Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha (PGC-1α), preserving mitochondrial integrity and membrane potential.
Conclusions:
- PEG300 demonstrates neuroprotective effects against CNS-OT, likely mediated by upregulating PGC-1α and enhancing mitochondrial health.
- These findings suggest PEG300 as a potential therapeutic agent for preventing and treating CNS-OT.
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