Acute ethanol intoxication in a model of traumatic brain injury: The protective role of moderate doses demonstrated by immunoreactivity of synaptophysin in hippocampal neurons

2004 ◽  
Vol 26 (1) ◽  
pp. 108-112 ◽  
Author(s):  
Ercan Türeci ◽  
Reza Dashti ◽  
Taner Tanriverdi ◽  
Galip Zihni Sanus ◽  
Buge Öz ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Hippocampal Neurons ◽  
Protective Role ◽  
Ethanol Intoxication ◽  
Acute Ethanol ◽  
Acute Ethanol Intoxication

Yings and Yangs of Acute Ethanol Intoxication in Experimental Traumatic Brain Injury

2005 ◽  
Vol 15 (1) ◽  
pp. 60-64 ◽  
Author(s):  
Merih Is ◽  
Taner Tanriverdi ◽  
Fevzullah Akyuz ◽  
Mustafa Onur Ulu ◽  
Nil Ustundag ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Ethanol Intoxication ◽  
Acute Ethanol ◽  
Acute Ethanol Intoxication ◽  
Experimental Traumatic Brain Injury

scholarly journals Acute Ethanol Gavage Attenuates Hemorrhage/Resuscitation-Induced Hepatic Oxidative Stress in Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
B. Relja ◽  
K. Wilhelm ◽  
M. Wang ◽  
D. Henrich ◽  
I. Marzi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ethanol Intoxication ◽  
Arterial Blood ◽  
Inos Protein Expression ◽  
Acute Ethanol ◽  
Acute Fatty Liver ◽  
Acute Ethanol Intoxication ◽  
Subsequent Resuscitation

Acute ethanol intoxication increases the production of reactive oxygen species (ROS). Hemorrhagic shock with subsequent resuscitation (H/R) also induces ROS resulting in cellular and hepatic damagein vivo. We examined the role of acute ethanol intoxication upon oxidative stress and subsequent hepatic cell death after H/R. 14 h before H/R, rats were gavaged with single dose of ethanol or saline (5 g/kg, EtOH and ctrl; H/R_EtOH or H/R_ctrl, resp.). Then, rats were hemorrhaged to a mean arterial blood pressure of30±2 mmHg for 60 min and resuscitated. Two control groups underwent surgical procedures without H/R (sham_ctrl and sham_EtOH, resp.). Liver tissues were harvested at 2, 24, and 72 h after resuscitation. EtOH-gavage induced histological picture of acute fatty liver. Hepatic oxidative (4-hydroxynonenal, 4-HNE) and nitrosative (3-nitrotyrosine, 3-NT) stress were significantly reduced in EtOH-gavaged rats compared to controls after H/R. Proapoptotic caspase-8 and Bax expressions were markedly diminished in EtOH-gavaged animals compared with controls 2 h after resuscitation. EtOH-gavage increased antiapoptotic Bcl-2 gene expression compared with controls 2 h after resuscitation. iNOS protein expression increased following H/R but was attenuated in EtOH-gavaged animals after H/R. Taken together, the data suggest that acute EtOH-gavage may attenuate H/R-induced oxidative stress thereby reducing cellular injury in rat liver.

The Protective Role of Nutraceuticals in Critically Ill Patients with Traumatic Brain Injury

2021 ◽  
pp. 243-253
Author(s):  
Farshid Rahimibashar ◽  
Masoum Khosh Fetrat ◽  
Keivan Gohari-Moghadam ◽  
Tannaz Jamialahmadi ◽  
Amirhossein Sahebkar
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Protective Role

Role of Hypophysis and Adrenals in Fatty Infiltration of Liver Resulting From Acute Ethanol Intoxication

1955 ◽  
Vol 184 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Samuel Mallov ◽  
Janet L. Bloch
Keyword(s):  
Liver Lipid ◽  
Fatty Infiltration ◽  
Female Rats ◽  
Ethanol Intoxication ◽  
Lipid Response ◽  
Acute Ethanol ◽  
Hypophysectomized Rats ◽  
Acute Ethanol Intoxication ◽  
Prior Administration

Acute ethanol intoxication was found to promote the fatty infiltration of liver in rats. The liver lipid concentrations gradually rose to peak values, then slowly returned to normal. The duration of the fatty infiltration, and the peak liver lipid values obtained, were functions of the dose of ethanol administered. Female rats showed a more severe fatty infiltration than did males, under the same conditions. The prior administration of large quantities of choline reduced the intensity of the fatty infiltration provoked by the ethanol. In contrast to intact animals, neither adrenalectomized nor hypophysectomized rats showed an accumulation of liver lipids as a result of acute ethanol intoxication. Adrenalectomized rats maintained on cortisone, and adrenal demedullated rats, however, showed the same liver lipid response to ethanol as did intact rats. Rats chronically intoxicated for a period of 30 days exhibited hypertrophy of the adrenals. Acute intoxication produced by isopropanol administration also resulted in the accumulation of liver lipid. It is suggested that ethanol intoxication may cause the mobilization of fat from the depots to the liver, and that pituitary and adrenal cortical hormones are involved in the mechanism of this mobilization.

scholarly journals Role of Melatonin in Traumatic Brain Injury and Spinal Cord Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Mehar Naseem ◽  
Suhel Parvez
Keyword(s):  
Traumatic Brain Injury ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Brain Injury ◽  
Protective Role ◽  
Secondary Injury ◽  
Severe Injuries ◽  
Cord Injury ◽  
Injured Part

Brain and spinal cord are implicated in incidences of two of the most severe injuries of central nervous system (CNS). Traumatic brain injury (TBI) is a devastating neurological deficit involving primary and secondary injury cascades. The primary and secondary mechanisms include complex consequences of activation of proinflammatory cytokines, cerebral edema, upregulation of NF-κβ, disruption of blood-brain barrier (BBB), and oxidative stress. Spinal cord injury (SCI) includes primary and secondary injury cascades. Primary injury leads to secondary injury in which generation of free radicals and oxidative or nitrative damage play an important pathophysiological role. The indoleamine melatonin is a hormone secreted or synthesized by pineal gland in the brain which helps to regulate sleep and wake cycle. Melatonin has been shown to be a versatile hormone having antioxidative, antiapoptotic, neuroprotective, and anti-inflammatory properties. It has a special characteristic of crossing BBB. Melatonin has neuroprotective role in the injured part of the CNS after TBI and SCI. A number of studies have successfully shown its therapeutic value as a neuroprotective agent in the treatment of neurodegenerative diseases. Here in this review we have compiled the literature supporting consequences of CNS injuries, TBI and SCI, and the protective role of melatonin in it.

scholarly journals The Role of BDNF in Experimental and Clinical Traumatic Brain Injury

2021 ◽  
Vol 22 (7) ◽  
pp. 3582
Author(s):  
David Gustafsson ◽  
Andrea Klang ◽  
Sebastian Thams ◽  
Elham Rostami
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Pharmacological Treatment ◽  
Clinical Studies ◽  
Underlying Mechanism ◽  
Protective Role ◽  
Bdnf Expression ◽  
Neural Repair ◽  
Mortality And Morbidity

Traumatic brain injury is one of the leading causes of mortality and morbidity in the world with no current pharmacological treatment. The role of BDNF in neural repair and regeneration is well established and has also been the focus of TBI research. Here, we review experimental animal models assessing BDNF expression following injury as well as clinical studies in humans including the role of BDNF polymorphism in TBI. There is a large heterogeneity in experimental setups and hence the results with different regional and temporal changes in BDNF expression. Several studies have also assessed different interventions to affect the BDNF expression following injury. Clinical studies highlight the importance of BDNF polymorphism in the outcome and indicate a protective role of BDNF polymorphism following injury. Considering the possibility of affecting the BDNF pathway with available substances, we discuss future studies using transgenic mice as well as iPSC in order to understand the underlying mechanism of BDNF polymorphism in TBI and develop a possible pharmacological treatment.

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