Melatonin Provides Neuroprotection Following Traumatic Brain Injury-Promoted Mitochondrial Perturbation in Wistar Rat

Salman, Mohammad; Kaushik, Pooja; Tabassum, Heena; Parvez, Suhel

doi:10.1007/s10571-020-00884-5

Cited by 20 publications

(14 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Section: Role Of Mitochondria In Secondary Injurymentioning

confidence: 95%

“…This dysregulation following injury have been well-documented in several models of TBI although differences in the exact nature of dysregulation are found between injury severities (Fischer et al, 2016 ; di Pietro et al, 2017 ). In a rat CCI model for moderate TBI, Salman et al ( 2020 ) found that the mitochondrial fraction of DRP1, the major protein necessary for fission increased while decreasing in the cytosolic fraction, indicating recruitment of DRP1 to the mitochondria post injury. Consequently, several studies have sought to intervene on DRP1 activity post-TBI in order to alleviate components of secondary injury.…”

Section: Age-related Inflammationmentioning

confidence: 99%

“…Functionally, they observed a decrease in fission activity confirmed by electron microscopy; this correlated with an increase in the number of viable neurons in the treated group. As a result, the treated rats also had improved performances on a variety of motor-behavior tasks (Salman et al, 2020 ). Previous papers have reported similar findings using various pharmacological interventions to prevent DRP1 driven fission post-TBI (Wu et al, 2016 , 2018 ; Song et al, 2019 ).…”

Section: Age-related Inflammationmentioning

confidence: 99%

See 2 more Smart Citations

A Levee to the Flood: Pre-injury Neuroinflammation and Immune Stress Influence Traumatic Brain Injury Outcome

Houle

Kokiko-Cochran

2022

Front. Aging Neurosci.

View full text Add to dashboard Cite

Increasing evidence demonstrates that aging influences the brain's response to traumatic brain injury (TBI), setting the stage for neurodegenerative pathology like Alzheimer's disease (AD). This topic is often dominated by discussions of post-injury aging and inflammation, which can diminish the consideration of those same factors before TBI. In fact, pre-TBI aging and inflammation may be just as critical in mediating outcomes. For example, elderly individuals suffer from the highest rates of TBI of all severities. Additionally, pre-injury immune challenges or stressors may alter pathology and outcome independent of age. The inflammatory response to TBI is malleable and influenced by previous, coincident, and subsequent immune insults. Therefore, pre-existing conditions that elicit or include an inflammatory response could substantially influence the brain's ability to respond to traumatic injury and ultimately affect chronic outcome. The purpose of this review is to detail how age-related cellular and molecular changes, as well as genetic risk variants for AD affect the neuroinflammatory response to TBI. First, we will review the sources and pathology of neuroinflammation following TBI. Then, we will highlight the significance of age-related, endogenous sources of inflammation, including changes in cytokine expression, reactive oxygen species processing, and mitochondrial function. Heightened focus is placed on the mitochondria as an integral link between inflammation and various genetic risk factors for AD. Together, this review will compile current clinical and experimental research to highlight how pre-existing inflammatory changes associated with infection and stress, aging, and genetic risk factors can alter response to TBI.

show abstract

Section: Role Of Mitochondria In Secondary Injurymentioning

confidence: 95%

Section: Age-related Inflammationmentioning

confidence: 99%

Section: Age-related Inflammationmentioning

confidence: 99%

See 1 more Smart Citation

A Levee to the Flood: Pre-injury Neuroinflammation and Immune Stress Influence Traumatic Brain Injury Outcome

Houle

Kokiko-Cochran

2022

Front. Aging Neurosci.

View full text Add to dashboard Cite

show abstract

“…It also reduces the degree of TBI-related inflammatory response, neuronal apoptosis, and oxidative stress [8]. A study on Wistar rats with TBI showed that melatonin administrated at a dose of 10 mg/kg body weight attenuated neuronal apoptosis and corrected mitochondrial perturbation by inhibiting mitochondrial fission [71]. Another experimental study showed that melatonin caused selective removal of damaged mitochondria by activating mitophagy, which was an important mechanism for reducing the severity of neuroinflammation after TBI [72].…”

Section: Brain Injury and Melatoninmentioning

confidence: 99%

Melatonin and the Brain–Heart Crosstalk in Neurocritically Ill Patients—From Molecular Action to Clinical Practice

Bekała

Płotek

Siwicka-Gieroba

et al. 2022

IJMS

View full text Add to dashboard Cite

Brain injury, especially traumatic brain injury (TBI), may induce severe dysfunction of extracerebral organs. Cardiac dysfunction associated with TBI is common and well known as the brain–heart crosstalk, which broadly refers to different cardiac disorders such as cardiac arrhythmias, ischemia, hemodynamic insufficiency, and sudden cardiac death, which corresponds to acute disorders of brain function. TBI-related cardiac dysfunction can both worsen the brain damage and increase the risk of death. TBI-related cardiac disorders have been mainly treated symptomatically. However, the analysis of pathomechanisms of TBI-related cardiac dysfunction has highlighted an important role of melatonin in the prevention and treatment of such disorders. Melatonin is a neurohormone released by the pineal gland. It plays a crucial role in the coordination of the circadian rhythm. Additionally, melatonin possesses strong anti-inflammatory, antioxidative, and antiapoptotic properties and can modulate sympathetic and parasympathetic activities. Melatonin has a protective effect not only on the brain, by attenuating its injury, but on extracranial organs, including the heart. The aim of this study was to analyze the molecular activity of melatonin in terms of TBI-related cardiac disorders. Our article describes the benefits resulting from using melatonin as an adjuvant in protection and treatment of brain injury-induced cardiac dysfunction.

show abstract

“…Previous studies showed a significant decrease in infarcted volume, protection of cells and improved outcome on neurobehavioral tests after administration of melatonin after ischemic brain injury in a rat model [15,16]. The role of melatonin on TBI has been studied too [17][18][19][20]; however, little is known about whether the administration of melatonin could promote the regeneration of neurons in rats with TBI. This study aims to investigate the effect of melatonin on regeneration of cortical neurons in rats with TBI.…”

Section: Introductionmentioning

confidence: 99%

Effect of melatonin on regeneration of cortical neurons in rats with traumatic brain injury

Chen

Ben

et al. 2020

CIM

View full text Add to dashboard Cite

Purpose: To investigate the effect of melatonin on regeneration of cortical neurons in rats with traumatic brain injury (TBI). Methods: Sprague-Dawley rats (n=36) were randomly divided into sham, TBI+vehicle and TBI+melatonin groups. Cerebral blood flow and cognitive function were observed via laser Doppler flowmetry and by Morris water maze testing, respectively. The serum malondialdehyde (MDA) and superoxide dismutase (SOD) levels were used to assess oxidative stress. Immunofluorescence and terminal deoxynucleotidyl transferase dUTP nick end labelling assay was used to observe the newborn neurons and apoptotic cells. Results: Cerebral blood flow in the TBI+melatonin group was higher than that of the TBI+vehicle group at one, 12, 24 and 48 h post-injury, but the difference was not statistically significant (P>0.05). The cognitive function of the rats was better in the TBI+melatonin group than the TBI+vehicle group (P

show abstract

Melatonin Provides Neuroprotection Following Traumatic Brain Injury-Promoted Mitochondrial Perturbation in Wistar Rat

Cited by 20 publications

References 57 publications

A Levee to the Flood: Pre-injury Neuroinflammation and Immune Stress Influence Traumatic Brain Injury Outcome

A Levee to the Flood: Pre-injury Neuroinflammation and Immune Stress Influence Traumatic Brain Injury Outcome

Melatonin and the Brain–Heart Crosstalk in Neurocritically Ill Patients—From Molecular Action to Clinical Practice

Effect of melatonin on regeneration of cortical neurons in rats with traumatic brain injury

Contact Info

Product

Resources

About