scholarly journals Neuroprotective Role of Curcumin Against Benzo[a]pyrene-Induced Neurodegeneration in Zebrafish

2021 ◽  
Vol 12 (6) ◽  
pp. 7311-7320
Keyword(s):  
Neuroprotective Effect ◽  
Curcuma Longa ◽  
Histological Study ◽  
Redox Homeostasis ◽  
Grey Zone ◽  
Adult Zebrafish ◽  
Zebrafish Brain ◽  
Group B ◽  
The Brain

Curcuma longa L. has been shown to exhibit neuroprotection in the brain. Curcuma longa L. has been used for its neuroprotective effect in humans of neurological disorders. The present study is aimed to evaluate the neuroprotective role of curcumin, a key component of Curcuma longa L., following exposure to waterborne B[a]P. Wild-type adult zebrafish (Danio rerio) were assigned as naïve, control (dimethyl sulfoxide), curcumin, B[a]P (Benzo[a]pyrene) and B[a]P+ curcumin group. B[a]P-induced altered antioxidant levels were enhanced by curcumin in the B[a]P+curcumin group. Findings showed that B[a]P induced anti-anxiety behavioral response and altered antioxidant activity in zebrafish is reduced by curcumin. The periventricular grey zone (PGZ) located on the optic tectum (TeO) in the zebrafish brain regulates anxiety-like behavior. Our histological study showed a significant increase in pyknotic neuronal counts in PGZ of TeO in adult zebrafish brain following B[a]P exposure and was improved by curcumin co-supplementation. Recent findings showed that curcumin improves glutathione production, an antioxidant necessary for maintaining redox homeostasis and shows a neuroprotective role in brain cells. The present study's findings address the potential role of curcumin co-supplementation as a herbal therapeutic against B[a]P-induced neurotoxicity in zebrafish.

scholarly journals Exploring the Use of Dimethyl Fumarate as Microglia Modulator for Neurodegenerative Diseases Treatment

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 700
Author(s):  
Maria Rosito ◽  
Claudia Testi ◽  
Giacomo Parisi ◽  
Barbara Cortese ◽  
Paola Baiocco ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Iron Homeostasis ◽  
Brain Injuries ◽  
Neuroprotective Effect ◽  
Redox Homeostasis ◽  
Dimethyl Fumarate ◽  
Redox Balance ◽  
Fumaric Acid Ester ◽  
The Central Nervous System

The maintenance of redox homeostasis in the brain is critical for the prevention of the development of neurodegenerative diseases. Drugs acting on brain redox balance can be promising for the treatment of neurodegeneration. For more than four decades, dimethyl fumarate (DMF) and other derivatives of fumaric acid ester compounds have been shown to mitigate a number of pathological mechanisms associated with psoriasis and relapsing forms of multiple sclerosis (MS). Recently, DMF has been shown to exert a neuroprotective effect on the central nervous system (CNS), possibly through the modulation of microglia detrimental actions, observed also in multiple brain injuries. In addition to the hypothesis that DMF is linked to the activation of NRF2 and NF-kB transcription factors, the neuroprotective action of DMF may be mediated by the activation of the glutathione (GSH) antioxidant pathway and the regulation of brain iron homeostasis. This review will focus on the role of DMF as an antioxidant modulator in microglia processes and on its mechanisms of action in the modulation of different pathways to attenuate neurodegenerative disease progression.

scholarly journals M211. NEUROPROTECTIVE EFFECT OF SHI-ZHEN-AN-SHEN-TANG, A CHINESE HERB FORMULA ON MICE EXPOSED TO CUPRIZONE

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S216-S217
Author(s):  
Chao Ma ◽  
Yan Wu ◽  
Pei Chen ◽  
Yuan Jia ◽  
Dongqing Yin ◽  
...  
Keyword(s):  
Low Dose ◽  
Neuroprotective Effect ◽  
Chinese Herb ◽  
Large Body ◽  
High Dose ◽  
Neuregulin 1 ◽  
The Brain ◽  
Different Doses ◽  
Medium Dose

Abstract Background Our previous study indicated a therapeutic effect of Shi-Zhen-An-Shen-Tang (SZAST), a Chinese herb formula, on schizophrenia, but the related mechanism is unknown(citation). A large body of evidence suggests the important role of white matter of the brain in the pathophysiology of schizophrenia. This study was designed to evaluate the effect of SZAST on schizophrenia with demyelinated mice. Methods Male C57BL/6 mice were given mixed cuprizone (CPZ, a copper chelator, 0.2 %, w/w) rodent chow for six successive weeks to induce demyelination. During the last two weeks, mice were given an oral gavage of saline, or SZAST of three different doses (a low dose of 5.5g·kg-1·d-1, a medium dose of 8.24g·kg-1·d-1, or a high dose of 10.98 g·kg-1·d-1), or quetiapine, respectively. Behavioral tests were conducted after the last treatment. Meanwhile, the expression of myelin basic protein (MBP) and neuregulin-1(NRG1) in the brain was tested by immunohistochemistry staining or Western Blot. Results Mice exposed to CPZ for six weeks showed obvious schizophrenia-like behaviors, including lower nest-building activity, sensory gating activity, and higher locomotor activity. CPZ-fed mice also displayed a lower myelin density in the corpus callosum, hippocampus, and cerebral cortex and a reduction of MBP and NRG1 protein in the hippocampus compared with controls. Both quetiapine and SZAST significantly alleviated the abnormal schizophrenia-like behaviors and the impairment of myelin sheath in CPZ-fed mice, however, SZAST with medium dose showed better neuroprotective effect than the low dose or the high dose of SZAST. Furthermore, the expression of NRG1protein in the hippocampus was slightly, but not significantly increased in all SZAST-treated and quetiapine-treated groups. Discussion These results indicate that the neuroprotective effect of SZAST in demyelinated mice might partially relate to remyelination in the hippocampus in CPZ-fed mice.

scholarly journals Melatonin and Ischemic Stroke: Mechanistic Roles and Action

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Syed Suhail Andrabi ◽  
Suhel Parvez ◽  
Heena Tabassum
Keyword(s):  
Ischemic Stroke ◽  
Brain Injury ◽  
Neurological Diseases ◽  
Neuroprotective Effect ◽  
Economic Loss ◽  
Protective Role ◽  
Physiological Processes ◽  
Cord Injury ◽  
The Brain

Stroke is one of the most devastating neurological disabilities and brain’s vulnerability towards it proves to be fatal and socio-economic loss of millions of people worldwide. Ischemic stroke remains at the center stage of it, because of its prevalence amongst the several other types attacking the brain. The various cascades of events that have been associated with stroke involve oxidative stress, excitotoxicity, mitochondrial dysfunction, upregulation of Ca2+level, and so forth. Melatonin is a neurohormone secreted by pineal and extra pineal tissues responsible for various physiological processes like sleep and mood behaviour. Melatonin has been implicated in various neurological diseases because of its antioxidative, antiapoptotic, and anti-inflammatory properties. We have previously reviewed the neuroprotective effect of melatonin in various models of brain injury like traumatic brain injury and spinal cord injury. In this review, we have put together the various causes and consequence of stroke and protective role of melatonin in ischemic stroke.

scholarly journals Role of glutamate transporters in redox homeostasis of the brain

2014 ◽  
Vol 73 ◽  
pp. 181-191 ◽  
Author(s):  
Stephanie M. Robert ◽  
Toyin Ogunrinu-Babarinde ◽  
Kenneth T. Holt ◽  
Harald Sontheimer
Keyword(s):  
Redox Homeostasis ◽  
Glutamate Transporters ◽  
The Brain

scholarly journals Neuron-glia interaction through Serotonin-BDNF-NGFR axis enables regenerative neurogenesis in Alzheimer’s model of adult zebrafish brain

2019 ◽  
Author(s):  
Prabesh Bhattarai ◽  
Mehmet Ilyas Cosacak ◽  
Violeta Mashkaryan ◽  
Sevgican Yilmaz ◽  
Stanislava Dimitrova Popova ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Experimental Models ◽  
Interleukin 4 ◽  
List Type ◽  
Adult Zebrafish ◽  
Bdnf Expression ◽  
Zebrafish Brain ◽  
Amyloid Toxicity ◽  
The Brain

AbstractIt was recently suggested that supplying the brain with new neurons could counteract Alzheimer’s disease. This provocative idea requires further testing in experimental models where the molecular basis of disease-induced neuronal regeneration could be investigated. We previously found that zebrafish stimulates neural stem cell (NSC) plasticity and neurogenesis in Alzheimer’s disease and could help to understand the mechanisms to be harnessed for develop new neurons in diseased mammalian brains. Here, by performing single-cell transcriptomics, we found that Amyloid toxicity-induced Interleukin-4 induces NSC proliferation and neurogenesis by suppressing the tryptophan metabolism and reducing the production of Serotonin. NSC proliferation was suppressed by Serotonin via downregulation of BDNF-expression in Serotonin-responsive periventricular neurons. BDNF enhances NSC plasticity and neurogenesis via NGFRA/NFkB signaling in zebrafish but not in rodents. Collectively, our results suggest a complex neuron-glia interaction that regulates regenerative neurogenesis after Alzheimer’s disease conditions in zebrafish.Key findings-Amyloid-induced Interleukin-4 suppresses Serotonin (5-HT) production in adult zebrafish brain-5-HT affects htr1-expresing neurons and suppresses bdnf expression-BDNF enhances plasticity in neural stem cells via NGFRA/NFkB signaling-BDNF/NGFRA signaling is a neuro-regenerative mechanism in zebrafish but not in mammals.

scholarly journals Testosterone May Hold Therapeutic Promise for the Treatment ofIschemic Stroke in Aging: A Closer Look at Laboratory Findings

2019 ◽  
Vol 9 (1) ◽  
pp. 48-55 ◽  
Author(s):  
Fereshteh Farajdokht ◽  
Mehdi Farhoudi ◽  
Alireza Majdi ◽  
Masumeh Zamanlu ◽  
Saeed Sadigh-Eteghad ◽  
...  
Keyword(s):  
Apoptotic Cell ◽  
Neuroprotective Effect ◽  
Cerebrovascular Disorders ◽  
Neuroprotective Activity ◽  
Laboratory Findings ◽  
Aging Men ◽  
Effective Therapeutic Strategy ◽  
The Brain

Male sex is more prone to cerebrovascular disorders, yet the exact role of androgens in cerebralischemia remains unclear. Here we reviewed current understanding of testosterone (TES)neuroprotective activity against ischemic stroke and mechanisms underlying these effects inaging. TES may exert a neuroprotective effect in aging through pathways including inhibition ofoxidant molecules production, enhancing the enzymatic antioxidant capacity of the brain andmodulation of apoptotic cell death. Given this, a better understanding of the neuroprotectiveroles of TES may propose an effective therapeutic strategy to improve the quality of life anddecrease androgen-related cerebrovascular problems in the aging men.

THE EFFECT OF SURGICAL ISOLATION OF THE HYPOTHALAMUS UPON REPRODUCTIVE FUNCTION IN THE FEMALE GUINEA-PIG

1971 ◽  
Vol 50 (3) ◽  
pp. 507-NP ◽  
Author(s):  
JEAN E. M. BUTLER ◽  
B. T. DONOVAN
Keyword(s):  
Guinea Pig ◽  
Histological Study ◽  
Reproductive Function ◽  
Mature Female ◽  
Corpora Lutea ◽  
Suprachiasmatic Nuclei ◽  
Anterior Border ◽  
Luteal Function ◽  
The Brain

SUMMARY Under stereotaxic guidance, the connexions between the hypothalamus and the rest of the brain were severed surgically in mature female guinea-pigs, and reproductive function was assessed by following the vaginal cycle and by histological study of the ovaries. Animals in which the hypothalamic island incorporated the suprachiasmatic nuclei, or in which the anterior connexions to the hypothalamus were severed by a cut placed just anterior to the suprachiasmatic nuclei, developed persistent vaginal oestrus. Such an anterior cut in the hypothalamus did not influence luteal function in hysterectomized animals. When the anterior border of a hypothalamic island, or an anterior cut through the hypothalamus, was caudal to the suprachiasmatic nuclei, oestrous cycles continued although they were slightly irregular. The ovaries contained corpora lutea. Severance of the posterior connexions to the hypothalamus did not alter the oestrous cycle. The role of the suprachiasmatic area in the generation of persistent vaginal oestrus is discussed.

scholarly journals Thiamine as a Possible Neuroprotective Strategy in Neonatal Hypoxic-Ischemic Encephalopathy

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 42
Author(s):  
Gian Pietro Sechi ◽  
Flaminia Bardanzellu ◽  
Maria Cristina Pintus ◽  
Maria Margherita Sechi ◽  
Maria Antonietta Marcialis ◽  
...  
Keyword(s):  
Neuroprotective Effect ◽  
Hypoxic Ischemic Encephalopathy ◽  
Neuroprotective Strategy ◽  
Pathophysiological Role ◽  
High Doses ◽  
The Many ◽  
The Brain ◽  
Thiamine Treatment ◽  
Ischemic Encephalopathy

On the basis that similar biochemical and histological sequences of events occur in the brain during thiamine deficiency and hypoxia/ischemia related brain damage, we have planned this review to discuss the possible therapeutic role of thiamine and its derivatives in the management of neonatal hypoxic-ischemic encephalopathy (HIE). Among the many benefits, thiamine per se as antioxidant, given intravenously (IV) at high doses, defined as dosage greater than 100 mg IV daily, should counteract the damaging effects of reactive oxygen and nitrogen species in the brain, including the reaction of peroxynitrite with the tyrosine residues of the major enzymes involved in intracellular glucose metabolism, which plays a key pathophysiological role in HIE in neonates. Accordingly, it is conceivable that, in neonatal HIE, the blockade of intracellular progressive oxidative stress and the rescue of mitochondrial function mediated by thiamine and its derivatives can lead to a definite neuroprotective effect. Because therapeutic hypothermia and thiamine may both act on the latent period of HIE damage, a synergistic effect of these therapeutic strategies is likely. Thiamine treatment may be especially important in mild HIE and in areas of the world where there is limited access to expensive hypothermia equipment.

Postoperative Epileptic Seizures in Children: Is the Brain Incision a Risk Factor?

Neurosurgery ◽  
2017 ◽  
Vol 82 (4) ◽  
pp. 465-472 ◽  
Author(s):  
Luca Massimi ◽  
Domenica Battaglia ◽  
Federico Bianchi ◽  
Simone Peraio ◽  
Elisabetta Peppucci ◽  
...  
Keyword(s):  
Risk Factor ◽  
Surgical Planning ◽  
Epileptic Seizures ◽  
Postoperative Management ◽  
The Other ◽  
Group A ◽  
Group B ◽  
The Brain

Abstract BACKGROUND Postoperative seizures (PSs) after neurosurgical operations are common but little is known about the role of surgical brain incision on their genesis. This topic has not been addressed so far. OBJECTIVE To verify if the corticotomy affects the risk of PSs and postoperative epilepsy (PE) in children. METHODS One hundred forty-three consecutive pediatric cases operated on for supratentorial lesions at the same institution in the last 15 yr have been retrospectively reviewed by dividing them into group A, 68 children who required brain corticotomy mainly for hemispheric tumors, and group B, 75 children treated through extracortical approaches mainly for suprasellar and optic tumors. Patients with possible “epileptic” biases, like preoperative seizures, were excluded. RESULTS No significant differences have been found between group A and B as far as incidence of PSs (11.7% vs 14.5%) and PE (4.5% vs 6.5%), timing, and type of seizures are concerned after a mean 6.8 yr follow-up. The size of corticotomy in group A (<3 cm2 vs >3 cm2) had no impact on epileptogenesis as well as the other variables considered in both groups (age, sex, extent of lesion resection). CONCLUSION This study shows that the surgical cortical “trauma” would not represent a risk factor for PSs and PE. According to the present analysis and the literature, other causes seem to be involved (namely, electrolytic imbalance and brain gliosis). This information is important for preoperative surgical planning and postoperative management. A validation by both adult series and prospective studies is needed.

scholarly journals The Interleukin-1β/CXCL1/2/Neutrophil Axis Mediates Host Protection against Group B Streptococcal Infection

2014 ◽  
Vol 82 (11) ◽  
pp. 4508-4517 ◽  
Author(s):  
C. Biondo ◽  
G. Mancuso ◽  
A. Midiri ◽  
G. Signorino ◽  
M. Domina ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Group B Streptococcus ◽  
Neutrophil Recruitment ◽  
Interleukin 1Β ◽  
Host Protection ◽  
Target Organs ◽  
Group B ◽  
The Brain ◽  
Deficient Mice

ABSTRACTPrevious studies have indicated that group B streptococcus (GBS), a frequent human pathogen, potently induces the release of interleukin-1β (IL-1β), an important mediator of inflammatory responses. Since little is known about the role of this cytokine in GBS disease, we analyzed the outcome of infection in IL-1β-deficient mice. These animals were markedly sensitive to GBS infection, with most of them dying under challenge conditions that caused no deaths in wild-type control mice. Lethality was due to the inability of the IL-1β-deficient mice to control local GBS replication and dissemination to target organs, such as the brain and the kidneys. Moreover, in a model of inflammation induced by the intraperitoneal injection of killed GBS, a lack of IL-1β was associated with selective impairment in the production of the neutrophil chemokines CXCL1 and CXCL2 and in neutrophil recruitment to the peritoneal cavity. Decreased blood neutrophil counts and impaired neutrophil recruitment to the brain and kidneys were also observed during GBS infection in IL-1β-deficient mice concomitantly with a reduction in CXCL1 and CXCL2 tissue levels. Notably, the hypersusceptibility to GBS infection observed in the immune-deficient animals was recapitulated by neutrophil depletion with anti-Gr1 antibodies. Collectively, our data identify a cytokine circuit that involves IL-1β-induced production of CXCL1 and CXCL2 and leads the recruitment of neutrophils to GBS infection sites. Moreover, our data point to an essential role of these cells in controlling the progression and outcome of GBS disease.

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