Progesterone protects against lipid peroxidation following traumatic brain injury in rats

1997 ◽  
Vol 31 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Robin L. Roof ◽  
Stuart W. Hoffman ◽  
Donald G. Stein
Keyword(s):  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Brain Injury

scholarly journals Peroxynitrite-Mediated Protein Nitration and Lipid Peroxidation in a Mouse Model of Traumatic Brain Injury

2004 ◽  
Vol 21 (1) ◽  
pp. 9-20 ◽  
Author(s):  
Edward D. Hall ◽  
Megan R. Detloff ◽  
Kjell Johnson ◽  
Nancy C. Kupina
Keyword(s):  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Brain Injury ◽  
Mouse Model ◽  
Protein Nitration

scholarly journals Heme Oxygenase-2 Protects against Lipid Peroxidation-Mediated Cell Loss and Impaired Motor Recovery after Traumatic Brain Injury

2003 ◽  
Vol 23 (9) ◽  
pp. 3689-3696 ◽  
Author(s):  
Edward F. Chang ◽  
Ronald J. Wong ◽  
Hendrik J. Vreman ◽  
Takuji Igarashi ◽  
Ethel Galo ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Brain Injury ◽  
Heme Oxygenase ◽  
Cell Loss ◽  
Motor Recovery

Marked Gender Effect on Lipid Peroxidation after Severe Traumatic Brain Injury in Adult Patients

2004 ◽  
Vol 21 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Hülya Bayir ◽  
Donald W. Marion ◽  
Ava M. Puccio ◽  
Stephen R. Wisniewski ◽  
Keri L. Janesko ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Gender Effect ◽  
Adult Patients

scholarly journals The possibilities of pharmacological correction of ademol oxidative stress in rates with traumatic brain injury

2021 ◽  
Vol 25 (2) ◽  
pp. 192-195
Author(s):  
S. I. Semenenko
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Brain Injury ◽  
Oxidative Degradation ◽  
Male Rats ◽  
Control Group ◽  
Nacl Solution ◽  
Amantadine Sulfate

Annotation. An important measure of intensive care in patients with traumatic brain injury (TBI) is the use of pharmacotherapeutic agents with antioxidant properties. The aim of this study was to evaluate the effect of ademol compared with amantadine sulfate and 0.9% NaCl solution on the course of oxidative stress in the brain of TBI rats. The experiments were performed on 28 white male rats weighing 160-190 g. The experimental TBI model of severe severity was caused by the action of a carbon dioxide flow under pressure created using a gas balloon pneumatic gun. The therapeutic effect of ademol on model TBI was evaluated with a 2 mg/kg dose. The pseudoperated animals and control group received a 0.9% solution of NaCl and amantadine sulfate at a dose of 2 ml/kg and 5 mg/kg i/v. Data were processed using StatPlus 2009. We used the parametric criterion of t-Student, non-parametric criterion of W. White, paired criterion Ť. Wilcoxon, Fisher's angular transformation at p <0,05. In the course of the experiment, it was found that treatment of rats with TBI ademol leads to a decrease in the activity of lipid peroxidation and oxidative degradation of proteins (p<0.05) and promotes the normalization of the activity of antioxidant enzymes in cells of traumatically damaged brain (p<0.05). The use of ademol compared to amantadine sulfate and 0.9% NaCl solution was accompanied by a more significant decrease in the activity of lipid peroxidation and oxidative degradation of proteins and an improvement in the level of antioxidant enzymes in damaged brain of animals with TBI (p<0.05).

Early Onset of Lipid Peroxidation After Human Traumatic Brain Injury

2001 ◽  
Vol 49 (5) ◽  
pp. 450-458 ◽  
Author(s):  
Luciano Cristofori ◽  
Barbara Tavazzi ◽  
Roberta Gambin ◽  
Roberto Vagnozzi ◽  
Carlo Vivenza ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Brain Injury ◽  
Early Onset

scholarly journals Prokineticin-2 prevents neuronal cell deaths in a model of traumatic brain injury

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Zhongyuan Bao ◽  
Yinlong Liu ◽  
Binglin Chen ◽  
Zong Miao ◽  
Yiming Tu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Cell Death ◽  
Brain Injury ◽  
Neuronal Degeneration ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Prokineticin 2

AbstractProkineticin-2 (Prok2) is an important secreted protein likely involved in the pathogenesis of several acute and chronic neurological diseases through currently unidentified regulatory mechanisms. The initial mechanical injury of neurons by traumatic brain injury triggers multiple secondary responses including various cell death programs. One of these is ferroptosis, which is associated with dysregulation of iron and thiols and culminates in fatal lipid peroxidation. Here, we explore the regulatory role of Prok2 in neuronal ferroptosis in vitro and in vivo. We show that Prok2 prevents neuronal cell death by suppressing the biosynthesis of lipid peroxidation substrates, arachidonic acid-phospholipids, via accelerated F-box only protein 10 (Fbxo10)-driven ubiquitination, degradation of long-chain-fatty-acid-CoA ligase 4 (Acsl4), and inhibition of lipid peroxidation. Mice injected with adeno-associated virus-Prok2 before controlled cortical impact injury show reduced neuronal degeneration and improved motor and cognitive functions, which could be inhibited by Fbxo10 knockdown. Our study shows that Prok2 mediates neuronal cell deaths in traumatic brain injury via ferroptosis.

scholarly journals Maintained high sustained serum malondialdehyde levels after severe brain trauma injury in non-survivor patients

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Leonardo Lorente ◽  
María M. Martín ◽  
Pedro Abreu-González ◽  
Luis Ramos ◽  
Juan J. Cáceres ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Intensive Care ◽  
Brain Injury ◽  
Observational Study ◽  
Glasgow Coma Scale ◽  
Area Under Curve ◽  
Injury Severity ◽  
Severe Tbi ◽  
Trauma Injury

Abstract Objective Higher blood malondialdehyde (biomarker of lipid peroxidation) levels in the first hours of traumatic brain injury (TBI) have been found in patients with a worst prognosis. The objective of this study was to determine whether serum malondialdehyde levels during the first week of severe TBI could be used as mortality biomarkers. This was a multicenter, prospective and observational study performed in six Spanish Intensive Care Units. We included patients with severe TBI (defined as Glasgow Coma Scale < 9), and with Injury Severity Score in non-cranial aspects < 9. We determined serum malondialdehyde concentrations at days 1, 4 and 8 of TBI. We stablished 30-day mortality as the end-point study. Results We found that serum malondialdehyde concentrations at days 1 (p < 0.001), 4 (p < 0.001), and 8 (p < 0.001) of TBI were higher in non-survivor (n = 34) than in survivor (n = 90) patients. We found an area under curve of serum malondialdehyde concentrations at days 1, 4, and 8 of TBI to predict 30-day mortality of 77% (p < 0.001), 87% (p < 0.001) and 84% (p < 0.001) respectively. Thus, the new and most relevant findings of our study were serum malondialdehyde levels during the first week of TBI could be used as mortality biomarkers.

scholarly journals Pharmacological inhibition of lipid peroxidation attenuates calpain-mediated cytoskeletal degradation after traumatic brain injury

2011 ◽  
Vol 117 (3) ◽  
pp. 579-588 ◽  
Author(s):  
Ayman G. Mustafa ◽  
Juan A. Wang ◽  
Kimberly M. Carrico ◽  
Edward D. Hall
Keyword(s):  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Brain Injury ◽  
Pharmacological Inhibition
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