scholarly journals The Beneficial Roles of SIRT1 in Neuroinflammation-Related Diseases

2020 ◽  
Vol 2020 ◽  
pp. 1-19
Author(s):  
Fangzhou Jiao ◽  
Zuojiong Gong
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Bacterial Infections ◽  
Molecular Mechanisms ◽  
Catalytic Mechanism ◽  
Critical Role ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Wide Range ◽  
Cord Injury

Sirtuins are the class III of histone deacetylases whose deacetylate of histones is dependent on nicotinamide adenine dinucleotide (NAD+). Among seven sirtuins, SIRT1 plays a critical role in modulating a wide range of physiological processes, including apoptosis, DNA repair, inflammatory response, metabolism, cancer, and stress. Neuroinflammation is associated with many neurological diseases, including ischemic stroke, bacterial infections, traumatic brain injury, Alzheimer’s disease (AD), and Parkinson’s disease (PD). Recently, numerous studies indicate the protective effects of SIRT1 in neuroinflammation-related diseases. Here, we review the latest progress regarding the anti-inflammatory and neuroprotective effects of SIRT1. First, we introduce the structure, catalytic mechanism, and functions of SIRT1. Next, we discuss the molecular mechanisms of SIRT1 in the regulation of neuroinflammation. Finally, we analyze the mechanisms and effects of SIRT1 in several common neuroinflammation-associated diseases, such as cerebral ischemia, traumatic brain injury, spinal cord injury, AD, and PD. Taken together, this information implies that SIRT1 may serve as a promising therapeutic target for the treatment of neuroinflammation-associated disorders.

scholarly journals Ganglioside GM1 Targets Astrocytes to Stimulate Cerebral Energy Metabolism

2021 ◽  
Vol 12 ◽  
Author(s):  
Charles Finsterwald ◽  
Sara Dias ◽  
Pierre J. Magistretti ◽  
Sylvain Lengacher
Keyword(s):  
Molecular Mechanisms ◽  
Neuroprotective Effect ◽  
Brain Diseases ◽  
Mitochondrial Activity ◽  
Ganglioside Gm1 ◽  
Neuroprotective Effects ◽  
Wide Range ◽  
Cord Injury ◽  
Clinical Benefits ◽  
The Brain

Gangliosides are major constituents of the plasma membrane and are known to promote a number of physiological actions in the brain, including synaptic plasticity and neuroprotection. In particular, the ganglioside GM1 was found to have a wide range of preclinical and clinical benefits in brain diseases such as spinal cord injury, Huntington’s disease and Parkinson’s disease. However, little is known about the underlying cellular and molecular mechanisms of GM1 in the brain. In the present study, we show that GM1 exerts its actions through the promotion of glycolysis in astrocytes, which leads to glucose uptake and lactate release by these cells. In astrocytes, GM1 stimulates the expression of several genes involved in the regulation of glucose metabolism. GM1 also enhances neuronal mitochondrial activity and triggers the expression of neuroprotection genes when neurons are cultured in the presence of astrocytes. Finally, GM1 leads to a neuroprotective effect in astrocyte-neuron co-culture. Together, these data identify a previously unrecognized mechanism mediated by astrocytes by which GM1 exerts its metabolic and neuroprotective effects.

scholarly journals First person – Mohd. Salman

2020 ◽  
Vol 13 (8) ◽  
pp. dmm046169
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Molecular Mechanisms ◽  
Drug Repurposing ◽  
Early Career ◽  
First Person ◽  
New Delhi ◽  
Neuroprotective Effects ◽  
Early Career Researchers ◽  
Selection Of

ABSTRACTFirst Person is a series of interviews with the first authors of a selection of papers published in Disease Models & Mechanisms, helping early-career researchers promote themselves alongside their papers. Mohd. Salman is first author on ‘Nrf2/HO-1 mediates the neuroprotective effects of pramipexole by attenuating oxidative damage and mitochondrial perturbation after traumatic brain injury in rats’, published in DMM. Mohd. is a PhD student in the lab of Prof. Suhel Parvez at Jamia Hamdard, New Delhi, India, investigating the cellular and molecular mechanisms involved in traumatic brain injury, ischemic stroke and neurodegenerative diseases, and exploring the avenue of drug repurposing with pre-clinical studies.

Molecular mechanisms of estrogen for neuroprotection in spinal cord injury and traumatic brain injury

2016 ◽  
Vol 27 (3) ◽  
pp. 271-281 ◽  
Author(s):  
Mrinmay Chakrabarti ◽  
Arabinda Das ◽  
Supriti Samantaray ◽  
Joshua A. Smith ◽  
Naren L. Banik ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Brain Injury ◽  
Molecular Mechanisms ◽  
Adaptive Immune System ◽  
Cord Injury ◽  
Clinical Benefits

AbstractEstrogen (EST) is a steroid hormone that exhibits several important physiological roles in the human body. During the last few decades, EST has been well recognized as an important neuroprotective agent in a variety of neurological disorders in the central nervous system (CNS), such as spinal cord injury (SCI), traumatic brain injury (TBI), Alzheimer’s disease, and multiple sclerosis. The exact molecular mechanisms of EST-mediated neuroprotection in the CNS remain unclear due to heterogeneity of cell populations that express EST receptors (ERs) in the CNS as well as in the innate and adaptive immune system. Recent investigations suggest that EST protects the CNS from injury by suppressing pro-inflammatory pathways, oxidative stress, and cell death, while promoting neurogenesis, angiogenesis, and neurotrophic support. In this review, we have described the currently known molecular mechanisms of EST-mediated neuroprotection and neuroregeneration in SCI and TBI. At the same time, we have emphasized on the recent in vitro and in vivo findings from our and other laboratories, implying potential clinical benefits of EST in the treatment of SCI and TBI.

scholarly journals FGF2 Attenuates Neural Cell Death via Suppressing Autophagy after Rat Mild Traumatic Brain Injury

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Chonghui Tang ◽  
Yudong Shan ◽  
Yilan Hu ◽  
Zhanjian Fang ◽  
Yun Tong ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Early Stage ◽  
Pharmacological Therapy ◽  
Tissue Loss ◽  
Neurological Deficits ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Mild Tbi ◽  
Beneficial Effects

Traumatic brain injury (TBI) can lead to physical and cognitive deficits, which are caused by the secondary injury process. Effective pharmacotherapies for TBI patients are still lacking. Fibroblast growth factor-2 (FGF2) is an important neurotrophic factor that can stimulate neurogenesis and angiogenesis and has been shown to have neuroprotective effects after brain insults. Previous studies indicated that FGF2’s neuroprotective effects might be related to its function of regulating autophagy. The present study investigated FGF2’s beneficial effects in the early stage of rat mild TBI and the underlying mechanisms. One hundred and forty-four rats were used for creating controlled cortical impact (CCI) models to simulate the pathological damage after TBI. Our results indicated that pretreatment of FGF2 played a neuroprotective role in the early stage of rat mild TBI through alleviating brain edema, reducing neurological deficits, preventing tissue loss, and increasing the number of surviving neurons in injured cortex and the ipsilateral hippocampus. FGF2 could also protect cells from various forms of death such as apoptosis or necrosis through inhibition of autophagy. Finally, autophagy activator rapamycin could abolish the protective effects of FGF2. This study extended our understanding of FGF2’s neuroprotective effects and shed lights on the pharmacological therapy after TBI.

scholarly journals Controlled Decompression Attenuates Compressive Injury following Traumatic Brain Injury via TREK-1-Mediated Inhibition of Necroptosis and Neuroinflammation

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Tao Chen ◽  
Xiao Qian ◽  
Jie Zhu ◽  
Li-Kun Yang ◽  
Yu-Hai Wang
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Hypertension ◽  
Cortical Neurons ◽  
Molecular Mechanisms ◽  
Neuronal Injury ◽  
K Channel ◽  
Protective Effects

Decompressive craniectomy is an effective strategy to reduce intracranial hypertension after traumatic brain injury (TBI), but it is related to many postoperative complications, such as delayed intracranial hematoma and diffuse brain swelling. Our previous studies have demonstrated that controlled decompression (CDC) surgery attenuates brain injury and reduces the rate of complications after TBI. Here, we investigated the potential molecular mechanisms of CDC in experimental models. The in vitro experiments were performed in a traumatic neuronal injury (TNI) model following compression treatment in primary cultured cortical neurons. We found that compression aggravates TNI-induced neuronal injury, which was significantly attenuated by CDC for 2 h or 3 h. The results of immunocytochemistry showed that CDC reduced neuronal necroptosis and activation of RIP3 induced by TNI and compression, with no effect on RIP1 activity. These protective effects were associated with decreased levels of inflammatory cytokines and preserved intracellular Ca2+ homeostasis. In addition, the expression of the two-pore domain K+ channel TREK-1 and its activity was increased by compression and prolonged by CDC. Treatment with the TREK-1 blockers, spadin or SID1900, could partially prevent the effects of CDC on intracellular Ca2+ metabolism, necroptosis, and neuronal injury following TNI and compression. Using a traumatic intracranial hypertension model in rats, we found that CDC for 20 min or 30 min was effective in alleviating brain edema and locomotor impairment in vivo. CDC significantly inhibited neuronal necroptosis and neuroinflammation and increased TREK-1 activation, and the CDC-induced protection in vivo was attenuated by spadin and SID1900. In summary, CDC is effective in alleviating compressive neuronal injury both in vitro and in vivo, which is associated with the TREK-1-mediated attenuation of intracellular Ca2+ overload, neuronal necroptosis, and neuroinflammation.

scholarly journals Traumatic Brain Injury: Effect of Litigation Status on Executive Functioning—A Pilot Study

2020 ◽  
Author(s):  
Simi Prakash K. ◽  
Rajakumari P. Reddy ◽  
Anna R. Mathulla ◽  
Jamuna Rajeswaran ◽  
Dhaval P. Shukla
Keyword(s):  
Traumatic Brain Injury ◽  
Working Memory ◽  
Depressive Symptoms ◽  
Brain Injury ◽  
Concept Formation ◽  
Verbal Working Memory ◽  
Self Report ◽  
Semantic Fluency ◽  
Set Shifting ◽  
Wide Range

AbstractTraumatic brain injury (TBI) is associated with a wide range of physiological, behavioral, emotional, and cognitive sequelae. Litigation status is one of the many factors that has an impact on recovery. The aim of this study was to compare executive functions, postconcussion, and depressive symptoms in TBI patients with and without litigation. A sample of 30 patients with TBI, 15 patients with litigation (medicolegal case [MLC]), and 15 without litigation (non-MLC) was assessed. The tools used were sociodemographic and clinical proforma, executive function tests, Rivermead Post-Concussion Symptom Questionnaire, and Beck Depression Inventory. Assessment revealed that more than 50% of patients showed deficits in category fluency, set shifting, and concept formation. The MLC group showed significant impairment on verbal working memory in comparison to the non-MLC group. The performance of both groups was comparable on tests of semantic fluency, visuospatial working memory, concept formation, set shifting, planning, and response inhibition. The MLC group showed more verbal working memory deficits in the absence of significant postconcussion and depressive symptoms on self-report measures.

Protective effects of zinc chelation in traumatic brain injury correlate with upregulation of neuroprotective genes in rat brain

2004 ◽  
Vol 355 (3) ◽  
pp. 221-225 ◽  
Author(s):  
Helen L Hellmich ◽  
Christopher J Frederickson ◽  
Douglas S DeWitt ◽  
Ricardo Saban ◽  
Margaret O Parsley ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Rat Brain ◽  
Protective Effects ◽  
Zinc Chelation
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