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Remote Ischemic Conditioning Reduced Acute Lung Injury After Traumatic Brain Injury in the Mouse
Maha Saber1,2, Amanda D Rice3, Immaculate Christie1,2
1Child Health, University of Arizona College of Medicine-Phoenix, Phoenix, Arizona.
Remote ischemic conditioning (RIC) reduced acute lung injury (ALI) after traumatic brain injury (TBI) in mice by regulating sphingosine-1-phosphate (S1P) pathways, preserving lung function.
Area of Science:
- Neuroscience
- Pulmonology
- Immunology
Background:
- Traumatic brain injury (TBI) can lead to acute lung injury (ALI), but the underlying mechanisms are not fully understood.
- Remote ischemic conditioning (RIC) is a potential therapeutic strategy for various injuries, including neurological damage.
Purpose of the Study:
- To investigate the efficacy of RIC in mitigating TBI-induced ALI.
- To explore the role of the sphingosine-1-phosphate (S1P) pathway in TBI-induced ALI and its modulation by RIC.
Main Methods:
- Male mice underwent diffuse TBI or sham injury, with or without prior RIC.
- Lung tissue, bronchoalveolar lavage (BAL) fluid, and blood were collected at 1 hour and 7 days post-injury.
- Histopathology, cellularity, and levels of S1P receptors and irisin were analyzed.
Main Results:
- TBI caused lung alveolar damage and increased neutrophil infiltration, which RIC prevented.
- RIC normalized neutrophil levels in BAL fluid of TBI mice.
- RIC inhibited TBI-induced increases in lung S1P receptor 3 and irisin-associated protein.
Conclusions:
- RIC may serve as a viable intervention to reduce TBI-induced ALI.
- RIC appears to protect lung function by modulating the S1P-dependent pathway.
- Early intervention with RIC could aid in the clinical management of TBI patients.
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