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TIGAR plays neuroprotective roles in KA-induced excitotoxicity through reducing neuroinflammation and improving
Si-Si Huang1, Yi-Chao Sheng1, Yi-Yue Jiang1
1Department of Pharmacology and Laboratory of Aging and Nervous Diseases and Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Abstract:
Excitotoxicity refers to the ability of excessive extracellular excitatory amino acids to damage neurons via receptor activation. It is a crucial pathogenetic process in neurodegenerative diseases. TP53 is confirmed to be involved in excitotoxicity. It is demonstrated that TP53 induced glycolysis and apoptotic regulator (TIGAR)-regulated metabolic pathway can protect against neuronal injury. However, the role of TIGAR in excitotoxicity and specific mechanisms is still unknown. In this study, an in vivo excitotoxicity model was constructed via stereotypical kainic acid (KA) injection into the striatum of mice. KA reduced TIGAR expression levels, neuroinflammatory responses and mitochondrial dysfunction. TIGAR overexpression could reverse KA-induced neuronal injury by reducing neuroinflammation and improving mitochondrial function, thereby exerting neuroprotective effects. Therefore, this study could provide a potential therapeutic target for neurodegenerative diseases.
Insights
TP53 induced glycolysis and apoptotic regulator (TIGAR) protects neurons from excitotoxicity. Overexpressing TIGAR reversed kainic acid-induced injury by reducing inflammation and improving mitochondrial function, offering a therapeutic target for neurodegenerative diseases.
Area of Science:
- Neuroscience
- Cell Biology
- Metabolic Pathways
Background:
- Excitotoxicity, caused by excessive excitatory amino acids, damages neurons and is implicated in neurodegenerative diseases.
- TP53 is known to be involved in excitotoxicity.
- The TP53 induced glycolysis and apoptotic regulator (TIGAR) pathway's role in excitotoxicity is unclear.
Purpose of the Study:
- To investigate the role of TIGAR in excitotoxicity.
- To elucidate the specific mechanisms by which TIGAR influences neuronal injury in excitotoxicity models.
- To evaluate TIGAR as a potential therapeutic target for neurodegenerative diseases.
Main Methods:
- An in vivo excitotoxicity model was established using kainic acid (KA) injection into the mouse striatum.
- TIGAR expression levels, neuroinflammation, and mitochondrial function were assessed.
- The effects of TIGAR overexpression on KA-induced neuronal injury were examined.
Main Results:
- Kainic acid injection reduced TIGAR expression, increased neuroinflammation, and caused mitochondrial dysfunction.
- Overexpression of TIGAR ameliorated KA-induced neuronal damage.
- TIGAR overexpression mitigated neuroinflammation and improved mitochondrial function.
Conclusions:
- TIGAR plays a neuroprotective role against excitotoxicity.
- TIGAR exerts its protective effects by modulating neuroinflammation and mitochondrial function.
- TIGAR represents a potential therapeutic target for neurodegenerative diseases.
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