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Alpha Lipoic Acid Mitigates TBI-Induced Neuroinflammation by Regulating S100B/STIM Signaling via NF-ƙB Pathway
Iqra Mazahir1, Bushra Wali2, Ahmed Shaney Rehman1
1Department of Medical Elementology & Toxicology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi, India.
Molecular Neurobiology
|July 1, 2026
Summary
Alpha-lipoic acid (ALA) demonstrates neuroprotective effects by reducing oxidative stress and inflammation following traumatic brain injury (TBI). This study shows ALA mitigates TBI-induced neuronal damage and cognitive impairments in a rat model.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Traumatic brain injury (TBI) is a significant cause of neurological deficits, often involving glutamate excitotoxicity and secondary injury pathways.
- Alpha-lipoic acid (ALA), a natural antioxidant, has demonstrated neuroprotective properties in models of neurodegenerative diseases like Alzheimer's and Parkinson's.
Purpose of the Study:
- To investigate the protective effects of Alpha-lipoic acid (ALA) against controlled cortical impact (CCI)-induced traumatic brain injury (TBI) in Wistar rats.
- To elucidate the molecular mechanisms underlying ALA's neuroprotection, focusing on glutamatergic and calcium signaling pathways.
Main Methods:
- TBI was induced using controlled cortical impact (CCI) in Wistar rats, followed by ALA administration.
- Neuroprotection was assessed via behavioral tests (Barnes maze, beam balance, grip strength, Y-maze), brain water content, and histological analysis (light microscopy, immunofluorescence, TEM).
- Gene and protein expression of key markers (S100B, NMDA receptor subunit 2B, EAAT, STIM, UCHL1, NF-κB, GFAP, Iba1) were analyzed using qRT-PCR and western blotting.
Main Results:
- ALA administration downregulated S100B and NMDA receptor subunit 2B (GRIN2B) mRNA expression, and TBI-induced alterations in excitatory amino acid transporter (EAAT) expression in the cerebral cortex.
- Protein levels of S100B, STIM, UCHL1, NF-κB, and GFAP were elevated in TBI rats, with ALA potentially mitigating some of these changes.
- ALA mitigated the increased microglial activation (Iba1+) observed in the TBI model.
Conclusions:
- Alpha-lipoic acid (ALA) exhibits significant neuroprotective effects in a rat model of traumatic brain injury (TBI).
- ALA's mechanism involves modulating glutamatergic pathways and reducing neuroinflammation, indicated by decreased microglial activation.
- These findings support ALA's potential as a therapeutic agent for mitigating TBI-induced neuronal damage and cognitive dysfunction.