Introduction::Traumatic spinal cord injury (TSCI) is a catastrophic insult to the central nervous
system (CNS) and often leaves patients with profound, long-term neurological disability. In this
study, we evaluated whether dexpanthenol, a vitamin B5 precursor, exerts neuroprotective effects in a rat
model of TSCI. We also sought to clarify the mechanisms that might account for any observed benefit,
focusing on pathways related to apoptosis, inflammation, oxidative stress, and ferroptosis.
Methods::We used Wistar albino rats and allocated them into four groups: Control, Sham, Trauma, and
Dexpanthenol. Animals in the sham group underwent laminectomy alone. In contrast, rats in the trauma
and dexpanthenol groups received a standardized contusion injury created by dropping a 10 g weight
from 10 cm onto the exposed spinal cord. Immediately after injury, we administered dexpanthenol intraperitoneally
(i.p.) to the treatment group. Neurological function was evaluated 24 h later using the Basso,
Beattie, and Bresnahan (BBB) locomotor rating scale. Biochemical analyses were performed on tissue
samples to measure markers of apoptosis (Caspase-3), inflammation (Myeloperoxidase, MPO), lipid peroxidation
(Malondialdehyde, MDA), oxidative stress (Xanthine Oxidase, XO, Catalase, CAT), and ferroptosis
(Glutathione, GSH, Glutathione Peroxidase 4, GPX4, Acyl-CoA Synthetase Long Chain Family
Member 4, ACSL4, and Solute Carrier Family 7 Member 11, SLC7A11). Moreover, we prepared hematoxylin
and eosin (H&E) stained sections and carried out a semi-quantitative histopathological evaluation
based on these slides.
Results::Relative to the sham condition, spinal cord contusion produced a clear functional deterioration,
with BBB locomotor scores dropping sharply and histopathological injury becoming more pronounced.
In parallel, the trauma group showed substantial biochemical increases in caspase-3, MPO, MDA, XO,
and ACSL4. In contrast, antioxidant and ferroptosis-related defenses were suppressed after injury, as reflected
by significantly lower CAT, GSH, GPX4, and SLC7A11 levels. Administration of dexpanthenol
shifted this profile. Animals receiving treatment performed better on the BBB scale than untreated trauma
rats, indicating a significant recovery of neurological function. Consistently, tissue damage on histology
was attenuated, pro-apoptotic and pro-oxidant markers (caspase-3, MPO, MDA, XO, and ACSL4)
were reduced, and the depleted protective factors (CAT, GSH, GPX4, and SLC7A11) were brought back
toward baseline in a statistically significant manner.
Discussion::The restoration of antioxidant defenses and the specific inhibition of lipid peroxidation
markers suggest that dexpanthenol's efficacy extends beyond general anti-inflammatory effects. By targeting
ferroptosis-associated molecular changes via the preservation of the GPX4/GSH axis, dexpanthenol
addresses a fundamental mechanism of secondary neuronal death. These findings highlight the
therapeutic relevance of stabilizing membrane lipids and cellular energetics in the acute phase of neurotrauma.
Conclusion::Taken together, our data suggest that dexpanthenol provides significant protection in the
setting of TSCI. The benefit seems to arise from a multi-pronged profile: it inhibits apoptosis and inflammation,
limits oxidative damage, and attenuates key components of the ferroptotic cascade. In light
of these converging effects, dexpanthenol warrants further investigation as a candidate therapy for TSCI.