Egg yolk peptides protect brain cells from oxidative stress

Have your competent? doctor get the EXACT PROTOCOL on this so you can benefit.

 Egg yolk peptides protect brain cells from oxidative stress

As the human lifespan increases, so too does the risk of developing neurological disorders such as Parkinson's disease, Alzheimer's disease, anxiety and depression. These disorders are often accompanied by an excess amount of reactive oxygen species, or ROS. ROS are generated in the body throughout normal processes and have their place in a functioning cellular ecosystem; however, when their numbers get too high, problems arise. Hyun-Dong Paik from Konkuk University and his team of researchers use short chains of amino acids found in egg yolk, phosvitin phosphopeptides, to assess the effects of consumable antioxidants in protection against the build-up of oxidative stress in human neuroblastoma cells.

Hyun-Dong Paik and his team's results were published in Food Science of Animal Products on July 1st, 2026.

Reactive oxygen species (ROS), such as hydrogen peroxide (H2O2), in excess can lead to oxidative-stress-induced cell death during metabolic processes, in turn having the potential to lead to mutation and protein damage, later leading to various diseases. While human bodies have ways of eliminating some of these oxidants through antioxidant enzymes like catalases, it is often an overwhelming and impossible job once these oxidants start to build up excessively. This is where external forms of antioxidants, taken in through diet or supplementation, can help the process.

Testing occurred on SH-SY-5Y cells using PPP from hydrolyzed, high-temperature mild-pressure (HTMP) treated chicken egg yolk. The hydrolyzing process breaks the large molecules into smaller ones that can more easily be absorbed by the cells. Different agents such as trypsin (T), Multifect 14L (M) and a combination of the two (TM) were studied, as well as a treatment using just the HTMP-treated material. Of these four, HTMP-TM proved itself to show the most promise in reducing ROS.

The results from the HTMP-TM treatment had the highest antioxidant activity as well as increased cell viability (up to 76.44% from 57.46% when pretreated with HTMP-TM four hours before H2O2 treatment) and reduced cell death in stressed SH-SY-5Y cells. This treatment method also exhibited reducing power (meaning PPPs reduce the amount of electron-donating happening, therefore reducing the "energy" allowing for unfavorable reactions to occur) and radical scavenging (finding and reducing free radicals, which are unstable and reactive, and can damage cells and DNA).

Other effects of PPPs include metal chelation, which binds metals in a stable ring for later safe removal from the body, and beta-carotene bleaching inhibition and lipid peroxidation inhibition, both of which are protective against oxidative stress. HTMP-TM treated PPPs show the most evidence of being both antioxidative and neuroprotective on SH-SY-5Y cells.

PPPs are promising functional ingredients against H2O2-induced neurotoxicity. However, more in vivo studies are needed to demonstrate the value of PPPs as value-added food/nutraceutical ingredients."

Hyun-Dong Paik, researcher at Konkuk University and author of the study

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Additional work also needs to be done to determine the dosage, delivery route and safety of PPPs in humans and animals, as well as work on the functional activities of PPPs to continue understanding their place and function as a potential antioxidant and neuroprotective addition for the prevention of neurodegenerative diseases.

Ji-Eun Lee and Hyun-Dong Paik of the Department of Food Science and Biotechnology of Animal Resources at Konkuk University, Jae Hoon Lee of the Department of Food Science & Technology at Jeonbuk National University, Dong Uk Ahn of the Department of Animal Science at Iowa State University and Kee-Tae Kim of the Research Center at WithBio contributed to this research.

The National Institute of Food and Agriculture/USDA partially supported this work.

Source:

Tsinghua University Press

Journal reference:

Lee, J. -E., et al. (2026). Antioxidative and neuroprotective effects of phosvitin phosphopeptides against H 2 O 2 -induced oxidative stress in SH-SY5Y cells. Food Science of Animal Products. DOI: 10.26599/FSAP.2026.9240169. https://www.sciopen.com/article/10.26599/FSAP.2026.9240169

Neuroprotective properties of transition metal dichalcogenide nanoflowers alleviate acute and chronic neurological conditions linked to mitochondrial dysfunction

 

Of course, your competent? doctor already knew about reactive oxygen species way back in 2005, and got research initiated. NO? So you don't have a functioning stroke doctor, do you?

Reactive oxygen species and the modulation of stroke June 2005

reactive oxygen species (9 posts to July 2014)

And now this maybe to prevent or treat Alzheimers and Parkinsons if your competent? doctor can get followup testing going

Neuroprotective properties of transition metal dichalcogenide nanoflowers alleviate acute and chronic neurological conditions linked to mitochondrial dysfunction

Author links open overlay panel, ,

https://doi.org/10.1016/j.jbc.2025.108498

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Mitochondrial dysfunction is an expected cause of etiology and progression in numerous human neurological pathologies, including stroke, Alzheimer's, and Parkinson's diseases. Therefore, a neuroprotective treatment is an urgent and unmet need. Transition metal dichalcogenide nanoflowers (TMD NFs) exhibit unique biological properties. However, neuroprotective properties of these nanomaterials remain poorly understood. In the current study, the biological effect of molybdenum disulfide and molybdenum diselenide TMD NFs on neurons and astrocytes was investigated. It was found that both nanomaterials lowered reactive oxygen species levels, reduced mitochondrial impairment, and increased mitochondrial biogenesis. Neuroprotective effects of both TMD NFs resulted from upregulation of the peroxisome proliferator-activated receptor gamma coactivator 1 alpha pathway, the biological system responsible for mitochondrial biogenesis. Furthermore, administration of TMD NFs to Caenorhabditis elegans extended lifespan of the nematodes. These results indicate that TMD NFs can be used as novel neuroprotective therapeutic agents against acute and chronic neurological condition linked to mitochondrial dysfunction.

Combating Reactive Oxygen Species (ROS) with Antioxidant Supramolecular Polymers

Of course your competent? doctor already knew about this way back in 2005, and got research initiated. NO? So you don't have a functioning stroke doctor, do you?

Reactive oxygen species and the modulation of stroke June 2005

reactive oxygen species (9 posts to July 2014)

Combating Reactive Oxygen Species (ROS) with Antioxidant Supramolecular Polymers

• Penelope E. Jankoski
• Zacchaeus M. Wallace
• Loria R. DiMartino
• Jessica Shrestha
• Ashe M. Davis
• Iyanuoluwani Owolabi
• Alex S. Flynt
• Tristan D. Clemons*

Open PDFSupporting Information (3)

Abstract

Reactive oxygen species (ROS) are highly damaging biological molecules significantly upregulated following major injuries or diseases such as heart attack, burn injury, and stroke. Despite promising preclinical results, traditional small-molecule antioxidant therapies have had limited success in clinical applications. In this study, we employed a macromolecular approach to combat ROS, demonstrating that tethering the potent biological antioxidant, glutathione, to a peptide amphiphile effectively consumes harmful extracellular radicals while preserving antioxidant and polymeric functionality. By neutralizing these radical species, we can protect vulnerable cells from acute ROS toxicity. This was validated by assessing cellular oxidative damage and survival in cell lines stimulated with tert-butyl hydroperoxide (tBHP) to induce ROS production. The antioxidant nanofibers achieved cell rescue at concentrations an order of magnitude lower than molecular glutathione, a direct result of the extracellular localization and enhancement in the proximal concentration of the glutathione moieties along the supramolecular polymer. These antioxidant supramolecular polymers offer proof of principle for a macromolecular strategy to combat the damaging effects of extracellular ROS associated with disease and injury, showcasing their efficacy at low concentrations and maintaining antioxidant capabilities when in the gelled state, providing for the potential of an antioxidant tissue regenerative scaffold.

Nanozymes: Potential Therapies for Reactive Oxygen Species Overproduction and Inflammation in Ischemic Stroke and Traumatic Brain Injury

 Of course your competent? doctor already knew about this way back in 2005, and got research initiated. NO? So you don't have a functioning stroke doctor, do you?

Reactive oxygen species and the modulation of stroke June 2005

The latest here:

Nanozymes: Potential Therapies for Reactive Oxygen Species Overproduction and Inflammation in Ischemic Stroke and Traumatic Brain Injury

• Yunfan Yang
• , 
• Zixiang Li
• , 
• Xiaochong Fan
• , 
• Chao Jiang
• , 
• Junmin Wang
• , 
• Yousef Rastegar-Kashkooli
• , 
• Tom J. Wang
• , 
• Junyang Wang
• , 
• Menglu Wang
• , 
• Nannan Cheng
• , 
• Xiqian Yuan
• , 
• Xuemei Chen*
• , 
• Bing Jiang*
• , and 
• Jian Wang*
• 
  

Cite this: ACS Nano 2024, XXXX, XXX, XXX-XXX

Publication Date:June 19, 2024

https://doi.org/10.1021/acsnano.4c03425

© 2024 American Chemical Society

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SUBJECTS:

• Apoptosis,
• Cells,
• Central nervous system,
• Peptides and proteins,
• Rodent models

ACS Nano

Abstract

Nanozymes, which can selectively scavenge reactive oxygen species (ROS), have recently emerged as promising candidates for treating ischemic stroke and traumatic brain injury (TBI) in preclinical models. ROS overproduction during the early phase of these diseases leads to oxidative brain damage, which has been a major cause of mortality worldwide. However, the clinical application of ROS-scavenging enzymes is limited by their short in vivo half-life and inability to cross the blood-brain barrier. Nanozymes, which mimic the catalytic function of natural enzymes, have several advantages, including cost-effectiveness, high stability, and easy storage. These advantages render them superior to natural enzymes for disease diagnosis and therapeutic interventions. This review highlights recent advancements in nanozyme applications for ischemic stroke and TBI, emphasizing their potential to mitigate the detrimental effect of ROS overproduction, oxidative brain damage, inflammation, and blood-brain barrier compromise. Therefore, nanozymes represent a promising treatment modality for ROS overproduction conditions in future medical practices.

Reactive Oxygen Species: Angels and Demons in the Life of a Neuron

How EXACTLY is your doctor ensuring oxidative damage from your stroke doesn't occur?

Reactive Oxygen Species: Angels and Demons in the Life ofa Neuron

Kasturi Biswas 1,2 , Kellianne Alexander 1,2 and Michael M. Francis 1,2,* 1 Department of Neurobiology, University of Massachusetts Chan Medical School, Worcester, MA 01605, USA; kasturi.biswas@umassmed.edu (K.B.); kellianne.alexander@umassmed.edu (K.A.) 2 Graduate Program in Neuroscience, Morningside Graduate School of Biomedical Sciences, UMass Chan Medical School, Worcester, MA 01605, USA * Correspondence: michael.francis@umassmed.edu 

Abstract: 

Reactive oxygen species (ROS) have emerged as regulators of key processes supporting neuronal growth, function, and plasticity across lifespan. At normal physiological levels, ROS perform important roles as secondary messengers in diverse molecular processes such as regulating neuronal differentiation, polarization, synapse maturation, and neurotransmission. In contrast, high levels of ROS are toxic and can ultimately lead to cell death. Excitable cells, such as neurons, often require high levels of metabolic activity to perform their functions. As a consequence, these cells are more likely to produce high levels of ROS, potentially enhancing their susceptibility to oxidative damage. In addition, because neurons are generally post-mitotic, they may be subject to accumulating oxidative damage. Thus, maintaining tight control over ROS concentration in the nervous system is essential for proper neuronal development and function. We are developing a more complete understanding of the cellular and molecular mechanisms for control of ROS in these processes. This review focuses on ROS regulation of the developmental and functional properties of neurons, highlighting recent in vivo studies. We also discuss the current evidence linking oxidative damage to pathological conditions associated with neurodevelopmental and neurodegenerative disorders. Keywords: synapse; oxidative stress; C. elegans; neuro

Emerging Roles of Oxidative Stress in Brain Aging and Alzheimer's Disease

 They talk of antioxidants, caloric restriction and physical activity reducing oxidative stress but give no clues that they have written EXACT REHAB PROTOCOLS to prevent this problem. So, if no protocols were written it is useless.

Emerging Roles of Oxidative Stress in Brain Aging and Alzheimer's Disease

 

Author links open overlay panelAndraIonescu-Tucker^a

Carl W.Cotman^a

https://doi.org/10.1016/j.neurobiolaging.2021.07.014Get rights and content

Under a Creative Commons license

open access

Highlights

•

Oxidative stress is involved in the progression of aging and Alzheimer's disease (AD)

•

Free radicals damage mitochondria, increasing production of toxic amyloid beta (Aβ)

•

DNA repair dysfunction is more severe in the AD brain than in the aged brain

•

Inhibiting oxidation-induced epigenetic changes can improve cognition and reduce Aβ

•

Long term exercise effectively reduces oxidative stress and improves cognition

Abstract

Reactive oxygen species (ROS) are metabolic byproducts that are necessary for physiological function but can be toxic at high levels. Levels of these oxidative stressors increase gradually throughout the lifespan, impairing mitochondrial function and damaging all parts of the body, particularly the central nervous system. Emerging evidence suggests that accumulated oxidative stress may be one of the key mechanisms causing cognitive aging and neurodegenerative diseases such as Alzheimer's disease (AD). Here, we synthesize the current literature on the effect of neuronal oxidative stress on mitochondrial dysfunction, DNA damage and epigenetic changes related to cognitive aging and AD. We further describe how oxidative stress therapeutics such as antioxidants, caloric restriction and physical activity can reduce oxidation and prevent cognitive decline in brain aging and AD. Of the currently available therapeutics, we propose that long term physical activity is the most promising avenue for improving cognitive health by reducing ROS while promoting the low levels required for optimal function.

Antioxidants Go After Secondary Injury in Brain Bleeds

 Good enough for at least a preliminary protocol? Or do we have to wait at least 50 years or never for followup to occur? Since we have NO STROKE LEADERSHIP, there is no specific person we can contact to ensure followup is done and protocols created. Stroke survivors will continue to be screwed until we overthrow the existing leadership failures in stroke.

Antioxidants Go After Secondary Injury in Brain Bleeds

Preliminary data show promise where no drugs have succeeded before

by Nicole Lou, Staff Writer, MedPage Today February 25, 2021

Reactive oxygen species (ROS) scavengers were modestly neuroprotective in the acute period of intracerebral hemorrhage (ICH), according to a small randomized trial.

Perihematomal edema (PHE) expanded less with a 14-day course of N-acetylcysteine and selenium in the neurological ICU compared with placebo, reported Seungjoo Lee, MD, PhD, of Asan Medical Center in Seoul, Korea, and colleagues. Their manuscript was published online in Stroke.

That was true for both the edema volume (mean 21.90 vs 30.66 mL, P<0.01) and the ratio of volume at 2 weeks to that at baseline (1.19 vs 2.05, P<0.01).

However, brain hemorrhage volumes came out similar at 2 weeks with the ROS scavenger and placebo (mean 20.90 vs 18.70, P=0.74).

ROS scavenger recipients did reach target sedation levels faster (mean 5.98 hours vs 8.42 hours, P<0.01) and have shorter ICU stays (6.46 days vs 12.66 days, P<0.01) compared with the placebo group.

Yet 30-day functional outcomes on the modified Ranking Scale (mRS) didn't improve more (scores 3.34 vs 3.53 with placebo), nor were total hospital stays shorter (20.28 vs 23.71 days).(so really no functional efficacy.)

"These results propose that our ROS scavengers are potent antioxidants with properties that mitigate PHE and functional outcomes (that's not what you said in the previous sentence.) in the acute period of patients with ICH," Lee's group maintained.

Like other critically-ill patients, people with ICH have oxidative stress that contributes to direct cellular injury. PHE is an imaging marker of secondary injury following ICH, and its clinical significance has been a subject of debate.

"Discovering treatments that mitigate secondary injury is a major unmet need in the uphill battle of reducing the global burden of death and disability from ICH," according to Ashkan Shoamanesh, MD, and Aristeidis Katsanos, MD, PhD, both of the Population Health Research Institute at McMaster University in Hamilton, Ontario.

Lee's trial joins a short list of ICH clinical randomized trials showing a reduction in PHE volume with intervention and thus "provides exciting novel results supporting the potential benefit and safety antioxidant therapy in this fight," the pair wrote in an accompanying editorial.

"Although [the investigators'] findings are too preliminary to be implemented in clinical practice at this time, they are promising, supported by sound biological rationale, and warrant further exploration in large-scale clinical trials," the editorialists concluded.

Lee's group noted that ICH accounts for 10% and 27% of strokes and is associated with very high mortality and morbidity rates that have not budged in 30 years. No proven acute ICH therapies exist to date, as trial after trial has failed to show benefits to proposed medical and surgical interventions.

Their single-blind, randomized trial was conducted at several Korean centers. Eligible patients had spontaneous ICH and secondary ICH due to vascular anomalies, venous thrombosis, neoplasms, or hemorrhagic infarction (i.e., cases where hematoma and PHE can be measured on CT).

Lee and colleagues randomized 123 people to ROS scavengers (N-acetylcysteine 2000 mg/d and selenium 1600 µg/d IV for 14 days) or placebo starting within 24 hours of admission.

ROS scavenger and placebo groups shared similar baseline characteristics, including age (mean 54.4 vs 56.1 years) and sex (men 64.9% vs 53%). Initial hemorrhage volumes (34.78 vs 36.71 mL) and PHE volumes (18.47 vs 19.09 mL) were also comparable.

Hypertensive ICH was the most common type of ICH, accounting for over 40% of cases. Cerebrovascular disease was the second most common cause and was observed in 30%.

Study investigators reported no serious adverse events attributed to the ROS scavengers.

Their reasons for choosing N-acetylcysteine and selenium for this study, they said, included the abundance of existing safety data, their widespread availability, and low cost when compared with other ROS scavengers like edaravone and glutathione.

On top of the small sample size and single-blind design, the study couldn't determine whether the observed effects of ROS scavengers were due to one alone or the combination of the two.

Another major limitation was the heterogeneous cohort of ICH subtypes studied, as Shoamanesh and Katsanos noted that "the pathophysiology of secondary ICH subtypes, such as hemorrhagic neoplasms and infarction, includes additional mechanisms of brain injury and edema that likely overshadow the relative contribution of the hemorrhage to neuroimaging and clinical outcomes."

Furthermore, the literature suggests that ICH patients will need to be followed for at least 6 months to detect meaningful differences in the mRS, the editorialists added.

Nonetheless, the preliminary data from Lee's group suggest that "PHE can be mitigated safely through supplemental antioxidant therapy with ROS scavengers," they said.

• 

  Nicole Lou is a reporter for MedPage Today, where she covers cardiology news and other developments in medicine. Follow

Disclosures

The study was funded by a grant from the National Research Foundation of Korea.

Lee, Shoamanesh, and Katsanos had no disclosures.

Primary Source

Stroke

Source Reference: Kim M, et al "Reactive oxygen species scavenger in acute intracerebral hemorrhage patients: a multicenter, randomized controlled trial" Stroke 2021; DOI: 10.1161/STROKEAHA.120.032266.

Secondary Source

Stroke

Source Reference: Shoamanesh A, Katsanos AH "Combatting secondary injury from intracerebral hemorrhage with supplemental antioxidant therapy" Stroke 2021; DOI: 10.1161/STROKEAHA.121.033849

 

Safflor Yellow B Attenuates Ischemic Brain Injury via Downregulation of Long Noncoding AK046177 and Inhibition of MicroRNA-134 Expression in Rats

Sounds interesting. Now to just get our incompetent doctors, stroke hospitals and stroke associations to get human research going. Or is this the responsibility of stroke survivors?  With NO STRATEGY AND NO LEADERSHIP, nothing ever gets done in stroke.

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING?

Safflor Yellow B Attenuates Ischemic Brain Injury via Downregulation of Long Noncoding AK046177 and Inhibition of MicroRNA-134 Expression in Rats

View this Special Issue

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Research Article | Open Access

Volume 2020 |Article ID 4586839 | 20 pages | https://doi.org/10.1155/2020/4586839

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Chaoyun Wang,¹ Hongzhi Wan,² Qiaoyun Wang,² Hongliu Sun,² Yeying Sun,² Kexin Wang,³ and Chunxiang Zhang⁴

¹Hearing and Speech Institute, Binzhou Medical University, Yantai 264003, China
²School of Pharmaceutical Sciences, Binzhou Medical University, Yantai 264003, China
³Third Class of Senior High School, No. 2 Middle School of Yantai Shandong, Yantai, China
⁴Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA

Academic Editor: Reggiani Vilela Gonçalves

Received08 Jul 2019

Revised11 Mar 2020

Accepted29 Apr 2020

Published04 Jun 2020

Abstract

Stroke breaks the oxidative balance in the body and causes extra reactive oxygen species (ROS) generation, leading to oxidative stress damage. Long noncoding RNAs (lncRNAs) and microRNAs play pivotal roles in oxidative stress-mediated brain injury. Safflor yellow B (SYB) was able to effectively reduce ischemia-mediated brain damage by increasing antioxidant capacity and inhibiting cell apoptosis. In this study, we investigated the putative involvement of lncRNA AK046177 and microRNA-134 (miR-134) regulation in SYB against ischemia/reperfusion- (I/R-) induced neuronal injury. I/R and oxygen-glucose deprivation/reoxygenation (OGD/R) were established in vivo and in vitro. Cerebral infarct volume, neuronal apoptosis, and protein expression were detected. The effects of SYB on cell activity, cell respiration, nuclear factor erythroid 2-related factor 2 (Nrf2), antioxidant enzymes, and ROS were evaluated. I/R or OGD/R upregulated the expression of AK046177 and miR-134 and subsequently inhibited the activation and expression of CREB, which caused ROS generation and brain/cell injury. SYB attenuated the effects of AK046177, inhibited miR-134 expression, and promoted CREB activation, which in turn promoted Nrf2 expression, and then increased antioxidant capacities, improved cell respiration, and reduced apoptosis. We suggested that the antioxidant effects of SYB were driven by an AK046177/miR-134/CREB-dependent mechanism that inhibited this pathway, and that SYB has potential use in reducing or possibly preventing I/R-induced neuronal injury.

1. Introduction

Stroke is an important cerebrovascular disease that afflicts many people worldwide and frequently causes death or long-term disability [1]. Ischemic stroke is the most common type, accounting for about 80% of all strokes [2, 3]. Brain injury is caused by disruption of blood flow to the brain and is characterized by oxidative stress. In addition, reoxygenation resulting from the restoration of blood flow exacerbates tissue damage [4].
Pathophysiologically, ischemia and reperfusion can inhibit the activity of endogenous antioxidant enzymes and promote the overproduction of reactive oxygen species (ROS) [5–7]. Previous studies have shown that antioxidants significantly reduce ischemic damage through the inhibition of ROS production [8–11]. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a reduction-oxidation- (redox-) sensitive transcription factor that binds to antioxidant response elements (ARE) and activates the transcription of antioxidant enzymes. Studies have shown that cysteine residues on protein Keap1 are oxidized by ROS, leading to the release and activation of Nrf2 [12, 13]. Thus, Nrf2 is a useful therapeutic target for reducing or preventing ROS damage in the brain following ischemia/reperfusion (I/R) injury. Cyclic AMP (cAMP) response element-binding protein (CREB) is a leucine zipper transcription factor that inhibits ROS generation and suppresses severe ischemic injury by upregulating brain-derived neurotrophic factor (BDNF) and Bcl-2 [14, 15].
MicroRNAs (miRNAs) are endogenous, short (≈22 nucleotides), noncoding single-strand RNAs that regulate gene expression at the posttranscriptional level by influencing the translation of specific target mRNAs. Recent research revealed that a variety of miRNAs play important roles in ischemic injury through the modulation of cellular redox reactions and mitochondrial function [16]. For example, downregulation of miR-134 enhances Bcl-2 expression and alleviates ischemic injury by regulating CREB activity [17].
Long noncoding RNAs (lncRNAs) play key roles in various cellular contexts under both physiological and pathological conditions, and they are involved in diverse biological processes such as RNA processing, modulation of apoptosis and invasion, and chromatin modification [18–20]. AK046177 is a 606-base pair (bp) noncoding RNA sequence derived from a gene sequence (from 116850844 to 116851448) located on chromosome 13.
Safflower yellow is the flavonoid compound extracted from Carthamus tinctorius L., which includes the components hydroxysafflor yellow A (HSYA) and safflor yellow B (SYB). It has been shown to effectively reduce oxidative stress-mediated damage [21, 22]. A study by Wang et al. demonstrated that HSYA significantly increases antioxidant enzyme activity by activating the cAMP/PKA signaling pathway [23]. SYB (Figure 1(a)) is a yellow amorphous powder with a purity of more than 98% by HPLC, and it is water soluble and has demonstrated protective effects in neuronal injury models induced by oxidative stress [24, 25]. However, its effect on brain injury induced by I/R remains to be investigated. This study tested whether SYB reduces I/R-mediated brain injury, and evaluated its potential mechanisms by studying changes in the expression of AK046177, miR-134, Nrf2, and CREB.

(a)

(b)

(c)

(d)

(e)

(f)

(g)

Figure 1 

Effect of safflor yellow B on neurological deficit score, infarction area, total motor score, and cAMP level. (a) Chemical structure of safflor yellow B. As shown in (b)–(e), rats were divided into six groups: sham, ischemia/reperfusion (I/R), AK046177 siRNA, AK046177 siRNA+miR-134 agomir, SYB, SYB+miR-134 agomir. Except for the sham group, all rats in the other groups had established ischemia for 1 h followed by reperfusion for 23 h. SYB and saline were administrated by tail vein continuously for three days before treatment with I/R, and miR-134 agomir and AK046177 siRNA were given via intracerebroventricular injection. The neurological deficit score of each rat was obtained according to Longa’s method. Infarct volumes were measured by staining brain sections with 2,3,5-triphenyltetrazolium chloride. (a) represents pathological changes of cerebral infarction ((a) sham; (b) I/R; (c) AK046177 siRNA; (d) AK046177 siRNA+miR-134 agomir; (e) SYB; (f) SYB+miR-134 agomir). (b) represents neurological deficit scores. (c) represents the infarction area. (d) represents total motor scores (n=8). As shown in (f)–(g), cAMP levels in the cerebral cortex and primary fetal cortical cells were detected using a ¹²⁵I-radioimmunoassay according to the method described by the manufacturer. Data are presented as mean ±S.D (n=8 in tissues;n=3 in cells). One-way ANOVA test was used to determine statistical significance.**P<.01 vs the sham group or the control group, ^## P<0.01 vs. the I/R group or the OGD/R group,^ΔP<0.05 or ^ΔΔP<0.01 vs. the AK046177 siRNA group, and ⁺P<0.05 or ⁺⁺P<0.01 vs. the SYB group.

Hydrogen Sulfide as a Factor of Neuroprotection during the Constitutive and Reparative Neurogenesis in Fish Brain

I'm sure your incompetent doctor and stroke hospital did absolutely nothing with this earlier research on hydrogen sulfide, commonly found in rotten eggs and human flatulence,

 8 posts on hydrogen sulfide back to Sept. 2012 helping with stroke prevention, reduction in stroke damage, protects stem cells and helps neurogenesis.

One line from these 8 posts which just proves how fucking incompetent your doctor is;

When the new compound was injected an hour after the simulation of a stroke, the authors observed about a 70 percent reduction in the severity of the observed stroke damage. March 2016. 

 The latest here and yes this is in fish, but can your doctor read and put two and two together?

Hydrogen Sulfide as a Factor of Neuroprotection during the Constitutive and Reparative Neurogenesis in Fish Brain

By Evgeniya V. Pushchina, Anatoly A. Varaksin and Dmitry K. Obukhov

Submitted: June 13th 2019Reviewed: November 19th 2019Published: December 24th 2019

DOI: 10.5772/intechopen.90547

Downloaded: 6

Abstract

The H2S-producing systems were studied in trout telencephalon, tectum, and cerebellum at 1 week after eye injury. The results of ELISA analysis have shown a 1.7-fold increase in the CBS expression at 1 week post-injury, as compared to the intact trout. In the ventricular and subventricular regions of trout telencephalon, CBS+ cells, as well as neuroepithelial and glial types, were detected. As a result of injury, the number of CBS+ neuroepithelial cells in the pallial and subpallial periventricular regions of the telencephalon increases. In the tectum, a traumatic damage leads to an increase in the CBS expression in radial glia with a simultaneous decrease in the number of CBS immunopositive neuroepithelial cells detected in intact animals. In the cerebellum, we revealed neuroglial interrelations, in which H2S is probably released from the astrocyte-like cells with subsequent activation of the neuronal NMDA receptors. The organization of the H2S-producing cell complexes suggests that the amount of glutamate produced in the trout cerebellum and its reuptake is controlled with the involvement of astrocyte-like cells, reducing its excitotoxicity. We believe that the increase in the number of H2S-producing cells constitutes a response to oxidative stress, and the overproduction of H2S neutralizes the reactive oxygen species.

Targeting Reperfusion Injury in the Age of Mechanical Thrombectomy

Hell, we still haven't targeted the reperfusion(neuronal cascade of death) injury after tPA administration. All because we have NO STROKE STRATEGY AND NO STROKE LEADERSHIP. Nothing is going to get solved until we get stroke survivors in charge.
http://stroke.ahajournals.org/content/49/7/1796?etoc=

Atsushi Mizuma, Midori A. Yenari

https://doi.org/10.1161/STROKEAHA.117.017286

Stroke. 2018;49:1796-1802

Originally published May 14, 2018

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• cytokines
• reactive oxygen species
• reperfusion injury

stroke

tissue-type plasminogen activator

Pharmacological recanalization with r-tPA (recombinant tissue-type plasminogen activator) has been the mainstay for acute ischemic stroke (IS) treatment.¹ Recent randomized controlled trials have additionally demonstrated the efficacy of mechanical thrombectomy (MT).^2–4 Although the restoration of blood flow is a major goal in acute treatment, if this occurs too late, worse damage can ensue, compared with no revascularization.⁵ This worsening results because of the generation of excess reactive oxygen species (ROS) which leads to direct cellular damage and indirect damage through the triggering of inflammation. Inflammation causes the generation of damaging immune mediators, effector molecules, and more ROS.⁶ ROS can also lead to apoptosis/necrosis via DNA/RNA damage and lipid peroxidation. This cycle is known as reperfusion injury (R/I; Figure). Experimental studies have shown that durations of >2- to 3-hours transient middle cerebral artery occlusion (tMCAO) lead to worsened injury compared with permanent MCAO.⁷ At the clinical level, delayed revascularization can sometimes lead to worsened outcomes.⁸ Hyperintense acute reperfusion marker seen on magnetic resonance imaging in some patients with stroke has been associated with hemorrhagic transformation (HTf) and clinical worsening, suggesting the existence of R/I in humans.⁹ Hence, adjunctive treatments to recanalization to target R/I has the potential to improve current outcomes while reducing complications of r-tPA.

Figure.

Reperfusion injury is thought to occur when a sudden influx of oxygenated blood introduces reactive oxygen species (ROS) into critically damaged ischemic brain. Ischemically damaged mitochondria become unable to efficiently neutralize ROS. Elevated ROS can directly damage DNA, RNA, and cause lipid peroxidation. ROS lead to immune cell activation, including brain resident microglia. Ischemic brain may also elaborate damage-associated molecular patterns (DAMPs) that act on Toll-like receptors (TLR) present on the surface of microglia. TLR activation triggers immune …

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