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Updated: Apr 20, 2026

Development of an Uncomplicated Mild Traumatic Brain Injury Model Modified by Weight-Drop Method and Evidenced by Magnetic Resonance Imaging
Published on: April 11, 2025
The effects of α-lipoic acid on immature rats with traumatic brain injury
1Department of Histology and Embryology, Dokuz Eylul University , Izmir , Turkey.
Insights
Alpha-lipoic acid (LA) may protect young rats from traumatic brain injury (TBI). LA treatment reduced neuronal death and apoptosis in brain regions affected by TBI, suggesting a potential therapeutic benefit.
Area of Science:
- Neuroscience
- Biochemistry
- Pediatric Medicine
Background:
- Traumatic brain injury (TBI) is a significant cause of death and disability in children.
- TBI induces oxidative stress, leading to neuronal damage and cell death (apoptosis).
- Alpha-lipoic acid (LA) is a potent antioxidant with free radical scavenging properties.
Purpose of the Study:
- To investigate the neuroprotective effects of alpha-lipoic acid (LA) in a rat pup model of traumatic brain injury (TBI).
- To assess the impact of LA on neuronal survival, apoptosis, and oxidative stress markers in specific brain regions following TBI.
Main Methods:
- A TBI contusion model was induced in 7-day-old male rat pups.
- Animals were randomly assigned to control, TBI, or TBI + LA treatment groups.
- LA was administered intragastrically for 2 days post-injury; brain tissues were analyzed for neuronal density, apoptosis (TUNEL, caspase-3), and oxidative stress markers (GPx, SOD, MDA).
Main Results:
- LA treatment significantly reduced TBI-induced neuronal death in the hippocampus, prefrontal cortex, and parietal cortex.
- The number of apoptotic cells (TUNEL- and caspase-3-positive) was decreased in LA-treated rats.
- LA administration enhanced the activity of antioxidant enzymes, glutathione peroxidase (GPx) and superoxide dismutase (SOD), in the prefrontal cortex.
Conclusions:
- Alpha-lipoic acid demonstrates neuroprotective effects against TBI in developing rats.
- LA mitigates neuronal apoptosis and enhances endogenous antioxidant defenses post-TBI.
- These findings suggest LA holds promise as a therapeutic agent for pediatric TBI.
Abstract:
Traumatic brain injury (TBI) is a leading cause of morbidity and mortality during childhood. TBI enhances formation of reactive oxygen species that cause neuron damage and apoptosis. α-Lipoic acid (LA) is a free radical scavenger and biological antioxidant. We investigated the effects of LA treatment on the parietal and prefrontal cortex, and on the hippocampal regions of the brain in 7-day-old rat pups that had been subjected to contusion injury. Forty-two male rats were divided randomly into a control group, a TBI group and a TBI + LA treated group. LA was administered 30 min after TBI through an intragastric tube once daily for 2 days. Forty-eight hours after TBI, the animals were sacrificed and tissues were examined for apoptosis and density of neurons. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) and active caspase-3 immunostaining were used to detect apoptosis. Glutathione peroxidase (GPx), superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels also were measured. Histological evaluation showed that LA treatment significantly reduced TBI-induced neuronal death in the hippocampus, prefrontal and parietal cortex; TUNEL- and caspase-3-positive cells also were decreased in the same regions. In addition, LA administration increased GPx and SOD activity in the prefrontal cortex. It appears that LA may be beneficial for TBI in rats.

