ArticleJournal of inflammation research2025
Fingolimod Suppresses NLRP3 Inflammasome Activation and Alleviates Oxidative Stress in Traumatic Brain Injury-Induced Acute Lung Injury.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Decoding mechanisms and protein markers in lung-brain axis.Respiratory research · 2025Review
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10 authors.
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Abstract
Background: Acute lung injury (ALI) is a serious yet common complication in patients with traumatic brain injury (TBI), often associated with poor prognosis. The development of TBI-induced ALI is closely associated with excessive oxidative stress and NLRP3 inflammasome activation. Fingolimod, an immunomodulatory agent, has been reported to attenuate inflammatory responses, restore blood-brain barrier integrity, reduce cerebral edema, and mitigate associated neurological deficits. Objective: This study aimed to investigate the mechanistic role of NLRP3 inflammasome activation in TBI-induced ALI and to evaluate the therapeutic potential of fingolimod in targeting this inflammatory pathway. Results: A rat TBI model was established using the classical free-fall method, and animals were treated with fingolimod (0.5 or 1 mg/kg) daily for three days. The TBI model rats presented with clear signs of histopathological pulmonary damage, an increase in the permeability of capillaries in the lung, and pulmonary edema that coincided with significantly increased NLRP3, caspase-1, and ASC expression in lung tissue samples. This overexpression of NLRP3 inflammasome machinery resulted in the release of IL-1β. Fingolimod treatment, however, reversed all of these effects such that it suppressed NLRP3 activity and normalized levels of IL-1β, leading to the alleviation of inflammation. In line with these results, LPS and nigericin (NLRP3 agonist)-treated NR8383 cells treated using fingolimod exhibited reductions in reactive oxygen species production and NLRP3 inflammasome activation. Conclusion: These findings suggest that NLRP3 inflammasome activation and oxidative stress are key mediators of TBI-induced ALI. Fingolimod exerts protective effects against this condition by inhibiting NLRP3 inflammasome activation, highlighting its potential as a therapeutic agent for TBI-associated pulmonary complications.
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