Title : The role of TNF-α in ischemic stroke
Abstract:
Ischemic stroke is one of the leading causes of mortality and long-term disability worldwide. Its pathogenesis is associated with the sudden occlusion of a cerebral artery, resulting in a critical reduction of blood flow and oxygen supply to brain tissue. This triggers a complex cascade of pathophysiological processes, including energy failure, glutamate-mediated excitotoxicity, oxidative stress, and activation of the inflammatory response.
Neuroinflammation plays a dual role in stroke: it contributes to neuronal damage while also initiating repair processes. These mechanisms involve numerous cytokines and immune mediators, including tumor necrosis factor alpha (TNF-α), a key proinflammatory cytokine that regulates immune responses, modulates blood–brain barrier permeability, and influences neuronal survival.
In the analyzed patient group, significant temporal changes in TNF-α levels were observed. The highest concentrations were recorded 24 hours after stroke onset, corresponding to the peak of the acute inflammatory response. Both 24-hour and 7-day measurements differed significantly from baseline values. However, no significant difference was found between day 1 and day 7, suggesting a sustained but relatively stable inflammatory activation.
Compared with the control group, TNF-α levels were significantly elevated only at 24 hours, whereas no statistically significant differences were observed at baseline or on day 7. This indicates that the increase in TNF-α is transient and primarily confined to the early acute phase.
No significant correlations were identified between TNF-α levels and clinical outcomes assessed using the NIHSS and mRS scales, suggesting limited utility of this cytokine as a prognostic biomarker.
In summary, TNF-α demonstrates a transient increase during the acute phase of ischemic stroke, peaking within the first 24 hours. Its elevated levels do not persist in later stages and do not show consistent associations with clinical outcomes. These findings suggest that TNF-α primarily serves as a marker of the early inflammatory response, with limited prognostic value in later stages of the disease.
