Berberine Protects Secondary Injury in Mice with Traumatic Brain Injury Through Anti-oxidative and Anti-inflammatory Modulation

Advancements in the critical care of patients with various forms of acute brain injury (traumatic brain injury, subarachnoid hemorrhage, stroke, etc.) in its current evolution recognizes that in addition to the initial insult, there is a secondary cascade of physiological events in the injured brain that contribute significantly to morbidity and mortality. Multimodality monitoring (MMM) in neurocritical care aims to recognize this secondary cascade in a timely manner. With early recognition, critical care of brain-injured patients may then be tailored to preventing and alleviating this secondary injury. MMM includes a variety of invasive and noninvasive techniques aimed at monitoring brain physiologic parameters such as intracranial pressure, perfusion, oxygenation, blood flow, metabolism, and electrical activity. This chapter provides an overview of these techniques and offers a practical guide to their integration and use in the intensive care setting.

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Traumatic brain injury in dogs and cats

Companion Animal ◽

10.12968/coan.2019.0015 ◽

2019 ◽

Vol 24 (9) ◽

pp. 480-487 ◽

Cited By ~ 1

Author(s):

Neus Elias ◽

Ana-Maria Rotariu ◽

Tobias Grave

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Traffic Accidents ◽

Road Traffic ◽

Companion Animals ◽

Treatment Strategies ◽

Secondary Injury ◽

Different Types ◽

Veterinary Surgeon ◽

Primary Injury

Traumatic brain injury is common in companion animals and can occur from many different types of trauma such as road traffic accidents or bites. Following the primary injury, which is beyond control of the clinician, secondary injury occurs minutes to days following the trauma. The secondary injury will lead to neuronal death, and is the focus of treatment strategies for the emergency veterinary surgeon. Treatment of traumatic brain injury includes nursing strategies, intravenous fluid therapy, hyperosmolar therapy and diuretics, pain management, maintenance of oxygenation and ventilation, temperature regulation, anticonvulsant therapy and glycaemic control. All of these are discussed in this clinical review.

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Inhibition of p21-activated kinase 1 by IPA-3 attenuates secondary injury after traumatic brain injury in mice

Brain Research ◽

10.1016/j.brainres.2014.08.026 ◽

2014 ◽

Vol 1585 ◽

pp. 13-22 ◽

Cited By ~ 4

Author(s):

Xinran Ji ◽

Wei Zhang ◽

Lihai Zhang ◽

Licheng Zhang ◽

Yiling Zhang ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Secondary Injury ◽

P21 Activated Kinase

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The Role of Free Radicals in Traumatic Brain Injury

Biological Research For Nursing ◽

10.1177/1099800411431823 ◽

2012 ◽

Vol 15 (3) ◽

pp. 253-263 ◽

Cited By ~ 24

Author(s):

Karen M. O’Connell ◽

Marguerite T. Littleton-Kearney

Keyword(s):

Traumatic Brain Injury ◽

Free Radicals ◽

Free Radical ◽

Brain Injury ◽

Current Knowledge ◽

Cellular Level ◽

Secondary Brain Injury ◽

Secondary Injury ◽

The Military

Traumatic brain injury (TBI) is a significant cause of death and disability in both the civilian and the military populations. The primary impact causes initial tissue damage, which initiates biochemical cascades, known as secondary injury, that expand the damage. Free radicals are implicated as major contributors to the secondary injury. Our review of recent rodent and human research reveals the prominent role of the free radicals superoxide anion, nitric oxide, and peroxynitrite in secondary brain injury. Much of our current knowledge is based on rodent studies, and the authors identified a gap in the translation of findings from rodent to human TBI. Rodent models are an effective method for elucidating specific mechanisms of free radical-induced injury at the cellular level in a well-controlled environment. However, human TBI does not occur in a vacuum, and variables controlled in the laboratory may affect the injury progression. Additionally, multiple experimental TBI models are accepted in rodent research, and no one model fully reproduces the heterogeneous injury seen in humans. Free radical levels are measured indirectly in human studies based on assumptions from the findings from rodent studies that use direct free radical measurements. Further study in humans should be directed toward large samples to validate the findings in rodent studies. Data obtained from these studies may lead to more targeted treatment to interrupt the secondary injury cascades.

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Peroxisome Proliferator-Activated Receptors: “Key” Regulators of Neuroinflammation after Traumatic Brain Injury

PPAR Research ◽

10.1155/2008/538141 ◽

2008 ◽

Vol 2008 ◽

pp. 1-7 ◽

Cited By ~ 27

Author(s):

Philip F. Stahel ◽

Wade R. Smith ◽

Jay Bruchis ◽

Craig H. Rabb

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Neuronal Cell Death ◽

Synthetic Cannabinoids ◽

Experimental Studies ◽

Neuronal Cell ◽

Peroxisome Proliferator ◽

Therapeutic Concept ◽

Anti Inflammatory ◽

Peroxisome Proliferator Activated Receptors

Traumatic brain injury is characterized by neuroinflammatory pathological sequelae which contribute to brain edema and delayed neuronal cell death. Until present, no specific pharmacological compound has been found, which attenuates these pathophysiological events and improves the outcome after head injury. Recent experimental studies suggest that targeting peroxisome proliferator-activated receptors (PPARs) may represent a new anti-inflammatory therapeutic concept for traumatic brain injury. PPARs are “key” transcription factors which inhibit NFκBactivity and downstream transcription products, such as proinflammatory and proapoptotic cytokines. The present review outlines our current understanding of PPAR-mediated neuroprotective mechanisms in the injured brain and discusses potential future anti-inflammatory strategies for head-injured patients, with an emphasis on the putative beneficial combination therapy of synthetic cannabinoids (e.g., dexanabinol) with PPARαagonists (e.g., fenofibrate).

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