scholarly journals Neuroprotective Effects of Resveratrol in Ischemic Brain Injury

NeuroSci ◽  
2021 ◽  
Vol 2 (3) ◽  
pp. 305-319
Author(s):  
Noelia D. Machado ◽  
Gorka Villena Armas ◽  
Mariana A. Fernández ◽  
Santiago Grijalvo ◽  
David Díaz Díaz
Keyword(s):  
Brain Injury ◽  
Cerebral Ischemia ◽  
De Novo ◽  
Neuroprotective Effect ◽  
Ischemic Brain Injury ◽  
In Vivo Models ◽  
Ischemic Brain ◽  
Number Of Patients

Cerebral ischemia represents the third cause of death and the first cause of disability in adults. This process results from decreasing cerebral blood flow levels as a result of the occlusion of a major cerebral artery. This restriction in blood supply generates low levels of oxygen and glucose, which leads to a decrease in the energy metabolism of the cell, producing inflammation, and finally, neurological deterioration. Currently, blood restoration of flow is the only effective approach as a therapy in terms of ischemic stroke. However, a significant number of patients still have a poor prognosis, probably owing to the increase in the generation of reactive oxygen species (ROS) during the reperfusion of damaged tissue. Oxidative stress and inflammation can be avoided by modulating mitochondrial function and have been identified as potential targets for the treatment of cerebral ischemia. In recent years, the beneficial actions of flavonoids and polyphenols against cerebrovascular diseases have been extensively investigated. The use of resveratrol (RSV) has been shown to markedly decrease brain damage caused by ischemia in numerous studies. According to in vitro and in vivo experiments, there is growing evidence that RSV is involved in several pathways, including cAMP/AMPK/SIRT1 regulation, JAK/ERK/STAT signaling pathway modulation, TLR4 signal transduction regulation, gut/brain axis modulation, GLUT3 up-regulation inhibition, neuronal autophagy activation, and de novo SUR1 expression inhibition. In this review, we summarize the recent outcomes based on the neuroprotective effect of RSV itself and RSV-loaded nanoparticles in vitro and in vivo models focusing on such mechanisms of action as well as describing the potential therapeutic strategies in which RSV plays an active role in cases of ischemic brain injury.

scholarly journals Intranasal Administration of Human MSC for Ischemic Brain Injury in the Mouse: In Vitro and In Vivo Neuroregenerative Functions

PLoS ONE ◽  
2014 ◽  
Vol 9 (11) ◽  
pp. e112339 ◽  
Author(s):  
Vanessa Donega ◽  
Cora H. Nijboer ◽  
Luca Braccioli ◽  
Ineke Slaper-Cortenbach ◽  
Annemieke Kavelaars ◽  
...  
Keyword(s):  
Brain Injury ◽  
Intranasal Administration ◽  
Ischemic Brain Injury ◽  
Ischemic Brain

scholarly journals β-Estradiol Protects Against Acidosis-Mediated and Ischemic Neuronal Injury by Promoting ASIC1a (Acid-Sensing Ion Channel 1a) Protein Degradation

Stroke ◽  
2019 ◽  
Vol 50 (10) ◽  
pp. 2902-2911 ◽  
Author(s):  
Renpeng Zhou ◽  
Tiandong Leng ◽  
Tao Yang ◽  
Feihu Chen ◽  
Wei Hu ◽  
...  
Keyword(s):  
Brain Injury ◽  
Protein Expression ◽  
Ion Channel ◽  
Ischemic Brain Injury ◽  
Estradiol Treatment ◽  
Ischemic Brain ◽  
Intracellular Ca ◽  
Ischemic Neuronal Injury

Background and Purpose— Sex differences in the incidence and outcome of stroke have been well documented. The severity of stroke in women is, in general, significantly lower than that in men, which is mediated, at least in part, by the protective effects of β-estradiol. However, the detailed mechanisms underlying the neuroprotection by β-estradiol are still elusive. Recent studies have demonstrated that activation of ASIC1a (acid-sensing ion channel 1a) by tissue acidosis, a common feature of brain ischemia, plays an important role in ischemic brain injury. In the present study, we assessed the effects of β-estradiol on acidosis-mediated and ischemic neuronal injury both in vitro and in vivo and explored the involvement of ASIC1a and underlying mechanism. Methods— Cultured neurons and NS20Y cells were subjected to acidosis-mediated injury in vitro. Cell viability and cytotoxicity were measured by methylthiazolyldiphenyl-tetrazolium bromide and lactate dehydrogenase assays, respectively. Transient (60 minutes) focal ischemia in mice was induced by suture occlusion of the middle cerebral artery in vivo. ASIC currents were recorded using whole-cell patch-clamp technique while intracellular Ca 2+ concentration was measured with fluorescence imaging using Fura-2. ASIC1a expression was detected by Western blotting and quantitative real-time polymerase chain reaction. Results— Treatment of neuronal cells with β-estradiol decreased acidosis-induced cytotoxicity. ASIC currents and acid-induced elevation of intracellular Ca 2+ were all attenuated by β-estradiol treatment. In addition, we showed that β-estradiol treatment reduced ASIC1a protein expression, which was mediated by increased protein degradation, and that estrogen receptor α was involved. Finally, we showed that the level of ASIC1a protein expression in brain tissues and the degree of neuroprotection by ASIC1a blockade were lower in female mice, which could be attenuated by ovariectomy. Conclusions— β-estradiol can protect neurons against acidosis-mediated neurotoxicity and ischemic brain injury by suppressing ASIC1a protein expression and channel function. Visual Overview— An online visual overview is available for this article.

Gingko biloba Extract (EGb 761) Prevents Increase of Bad-Bcl-XL Interaction Following Cerebral Ischemia

2009 ◽  
Vol 37 (05) ◽  
pp. 867-876 ◽  
Author(s):  
Phil-Ok Koh
Keyword(s):  
Brain Injury ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Neuroprotective Effect ◽  
Ischemic Brain Injury ◽  
Egb 761 ◽  
Adult Rats ◽  
Male Adult ◽  
Ischemic Brain ◽  
Gingko Biloba

A standardized extract of Gingko biloba, EGb 761, has been shown to exert a neuroprotective effect against permanent and transient focal cerebral ischemia. This study investigated whether EGb 761 modulates Bcl-2 family proteins in ischemic brain injury. Male adult rats were treated with EGb 761 (100 mg/kg) or vehicle prior to middle cerebral artery occlusion (MCAO), brain tissues were collected 24 hours after MCAO. EGb761 administration significantly decreased the number of TUNEL-positive cells in the cerebral cortex. Ischemic brain injury induced decrease of Bcl-2 and Bcl- X L levels. EGb 761 prevented not only the injury-induced decrease of Bcl-2 and Bcl- X L levels, but also the injury-induced increase of Bax. Moreover, in the presence of EGb 761, the interaction of Bad and Bcl- X L decreased compared to that of vehicle-treated animals. In addition, EGb 761 prevented the injury-induced increase of cleaved PARP. The finding suggests that EGb 761 prevents cell death against ischemic brain injury and EGb 761 neuroprotection is affected by preventing the injury-induced increase of Bad and Bcl- X L interaction.

Neuroprotective effects of topiramate and memantine in combination with hypothermia in hypoxic-ischemic brain injury in vitro and in vivo

2018 ◽  
Vol 668 ◽  
pp. 103-107 ◽  
Author(s):  
Elisa Landucci ◽  
Luca Filippi ◽  
Elisabetta Gerace ◽  
Serena Catarzi ◽  
Renzo Guerrini ◽  
...  
Keyword(s):  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Neuroprotective Effects ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

Abstract W P243: Multiple Therapeutic Effects of Progranulin on Experimental Acute Ischemic Stroke

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Masato Kanazawa ◽  
Kunio Kawamura ◽  
Tetsuya Takahashi ◽  
Minami Miura ◽  
Yoshinori Tanaka ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cerebral Ischemia ◽  
Growth Factor ◽  
Therapeutic Potential ◽  
Focal Cerebral Ischemia ◽  
Dynamic Change ◽  
Therapeutic Effects ◽  
Ischemic Brain Injury ◽  
In Vivo Models ◽  
Ischemic Brain

Introduction: In central nervous system, progranulin (PGRN), a glycoprotein growth factor, is considered to play crucial roles in maintaining physiological functions, and mutations in PGRN gene cause TAR DNA-binding protein-43 (TDP-43)-positive frontotemporal lobar degeneration. Although several studies reported that PGRN plays protective roles against ischemic brain injury, it remains unknown the precise mechanisms by which PGRN exerts protective effects on the ischemic brain injury. Methods: We determined the temporal changes of expression and localization of PGRN after ischemia as well as therapeutic effects of PGRN on ischemic brain injury using in vitro and in vivo models. Results: First, we demonstrated a dynamic change of PGRN expression in ischemic Sprague-Dawley rats, including increased levels of PGRN expression in microglia within the ischemic core, and increased level of PGRN expression in survived neurons as well as induction of PGRN expression in endothelial cells within the ischemic penumbra. Second, we demonstrated that PGRN could protect against acute focal cerebral ischemia by variety of mechanisms including via attenuation of blood-brain barrier disruption, suppression of neuroinflammation, and neuroprotection: we found that PGRN may regulate vascular permeability via vascular endothelial growth factor (VEGF), that PGRN may suppress neuroinflammation after ischemia via anti-inflammatory interleukin-10 (IL-10) in microglia, and that neuroprotective effect of PGRN may be explained in part by inhibition of cytoplasmic redistribution of TDP-43 using PGRN knock-out mice (C57Bl/6 background). Finally, we demonstrated the therapeutic potential of PGRN against acute focal cerebral ischemia using a rat autologous thromboembolic model with delayed tissue plasminogen activator (tPA) treatment. Intravenously administered recombinant PGRN reduced volumes of cerebral infarct and edema, suppressed hemorrhagic transformation, and improved motor outcome (P = 0.007, 0.038, 0.007, and 0.004, respectively). Conclusions: PGRN may be a novel therapeutic target that provides vascular protection, anti-neuroinflammation, and neuroprotection related in part to VEGF, IL-10, and TDP-43, respectively.

scholarly journals In Vivo and in Vitro Evaluation of the Anti-inflammatory Effect of Thymoquinone Toward Ischemic Brain Injury Alleviation via Nrf2/HO-1 Pathway

2020 ◽  
Author(s):  
Nashwa Amin ◽  
Xiaoxue Du ◽  
Shijia Chen ◽  
Qiannan Ren ◽  
Azhar Badry ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Brain Damage ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Chronic Dose ◽  
The Brain

Abstract Background - In recent years, considerable efforts have been devoted to exploring effective therapy for cerebral ischemia. Reactive oxygen species (ROS) mediated - inflammation plays a crucial role in ischemic brain injury. Triptolide (TP) has been widely used for ischemic therapy although administrating a chronic dose of this therapy may cause serious drawbacks and higher liver toxicity. Considering these critical side effects, here we demonstrate the employment of thymoquinone (TQ) as a new alternative drug for alleviating ischemic brain damage via suppression of inflammatory cytokines by inducing Nrf2/HO-1 under a chronic dose without toxicity. Methods- We assessed a photo-thrombosis mouse model of focal cerebral ischemia to investigate the impact of the chronic dose of TQ to alleviates ischemic brain damage, meanwhile, we used Pc12 to determine the efficiency of TQ to attenuate the OGD/R induces cell death. Results- Our in vivo and in vitro results indicate that the administration of TQ drug can sufficiently mitigate the brain damage after stroke by increasing the Nrf2/HO-1 expression and thereby modulate the cell death and inflammation resulting from cerebral ischemia. The observation based on YFP mice elucidates the role of TQ therapy in recovering the brain status after injury through increasing the dendrite spines density and the ratio of YFP reporter cells with NeuN expression. Conclusions- Our study is the first to focus on the crucial role of the Nrf2/HO-1 pathway as a promising ischemic therapy under a chronic dose of TQ by increasing proliferating protein expression, decreasing inflammation and neuronal cell death as well as controlling the autophagy process.

scholarly journals Effect of curcumin in the acute phase of ischemia in chronic cerebral hypoperfusion in rats

2018 ◽  
Vol 17 (1) ◽  
pp. 69-73
Author(s):  
N. S. Shcherbak ◽  
M. A. Popovetskiy ◽  
G. Yu. Yukina ◽  
M. M. Galagudza
Keyword(s):  
Brain Injury ◽  
Acute Phase ◽  
Wistar Rats ◽  
Neuroprotective Effect ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Ischemic Brain Injury ◽  
Protective Effects ◽  
Single Application ◽  
Ischemic Brain

Curcumin presents antioxidant and anti-inflammatory properties and can be considered as a neuroprotector. Data on doses and duration of application of curcumin to achieve protective effects in various types of ischemic brain injury is controversial. The purpose was to study the neuroprotective properties of curcumin in the acute phase of ischemia in chronic cerebral hypoperfusion in rats. It is shown that a single application of curcumin (300 mg/kg, i.p.) is not has neuroprotective effect in the acute phase of ischemia in chronic hypoperfusion in Wistar rats. The results allow to conclude that the neuroprotective effect of a single application of curcumin.

Sign in / Sign up

Export Citation Format

Share Document