ArticleInflammopharmacology2026
Syringic acid exerts neuroprotective effect in a rat model of traumatic brain injury through modulation of the MAPK signaling pathway.
Article in Inflammopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Traumatic brain injury is a leading cause of disability and mortality worldwide, often resulting in long-term cognitive, motor, and emotional impairments. The injury initiates a cascade of secondary injury mechanisms, including oxidative stress, neuroinflammation, and neuronal apoptosis, that exacerbate long-term functional deficits. The present study investigates the neuroprotective potential of Syringic acid, a naturally occurring polyphenolic compound, against traumatic brain injury -induced pathophysiology in wistar rats. Traumatic brain injury was induced via a fluid percussion injury model, and rats were subsequently treated orally with syringic acid at 25, 50, and 100 mg/kg doses for 14 days. Behavioral assessments, including grip strength, rotarod, morris water maze, and open field tests, indicated greater improvements were observed at higher doses in motor coordination and spatial memory compared with injured controls. Biochemical analysis showed that syringic acid significantly reduced lipid peroxidation and restored levels of endogenous antioxidants such as catalase and glutathione. Neurochemical assays indicated normalization of glutamate and gamma-aminobutyric acid levels. ELISA-based assessments showed decreased pro-inflammatory cytokines (Tumor Necrosis Factor- alpha, Interleukin-1 beta, and Interleukin-6), while immunohistochemistry demonstrated reduced expression of the apoptotic marker p38 mitogen-activated protein kinase. Histopathological analysis showed reduced cortical neuronal damage in syringic acid -treated groups, particularly at 100 mg/kg. These findings suggest a potential neuroprotective role for syringic acid in traumatic brain injury -induced neurological dysfunction by modulating oxidative stress, inflammation, and apoptosis. The dose-dependent neuroprotective effects of syringic acid support its potential as a promising therapeutic candidate for traumatic brain injury. However, further mechanistic and long-term studies are required to establish the translational relevance of these finding.
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