Enoxaparin Attenuates Acute Lung Injury and Inflammasome Activation after Traumatic Brain Injury.

Journal of Neurotrauma
Nadine A KerrRobert W Keane

Abstract

Traumatic brain injury (TBI) patients frequently develop cardiopulmonary system complications such as acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). However, the mechanism by which TBI causes ALI/ARDS is not fully understood. Here, we used a severe TBI model to examine the effects of a low-molecular-weight heparin, enoxaparin, on inflammasome activation and lung injury damage. We investigated whether enoxaparin inhibits ALI and inflammasome signaling protein expression in the brain and lungs after TBI in mice. C57/BL6 mice were subjected to severe TBI and were treated with vehicle or 1 mg/kg of enoxaparin 30 min after injury. Lung and brain tissue were collected 24 h post-TBI and were analyzed by immunoblotting for expression of the inflammasome proteins, caspase-1 and interleukin (IL)-1β. In addition, lung tissue was collected for histological analysis to determine ALI scoring and neutrophil and macrophage infiltration post-injury. Our data show that severe TBI induces increased expression of inflammasome proteins caspase-1 and IL-1β in the brain and lungs of mice after injury. Treatment with enoxaparin attenuated inflammasome expression in the brain and lungs 24 h after injury. Enoxaparin significantly de...Continue Reading

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Citations

Jan 27, 2021·Trends in Neurosciences·Alan I FadenRebecca J Henry
May 1, 2021·Cells·Brianna Cyr, Juan Pablo de Rivero Vaccari

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Methods Mentioned

BETA
nuclear translocation

Software Mentioned

GraphPad
ARRIVE
Prism
GraphPad Prism

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Brain Injury & Trauma

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