Apoptosis infarct size ischemia reperfusion. Medical search. Frequent questions

The pathophysiological nature of MIRI is the short-term disturbance of myocardial energy and metabolism caused by reflow after ischemia and hypoxia in the coronary artery and the dynamic changes in apoptosis and the prosurvival signaling pathways in response to related injury factors. (hindawi.com)

Cerebral ischemia-reperfusion injury (CIRI) refers to the phenomenon that the ischemic injury of brain leads to the injury of brain cells, and ischemic injury is further aggravated after the recovery of blood reperfusion. (sciencegate.app)
Cerebral ischemia-reperfusion injury (CIRI) caused by ischemic stroke seriously affects the prognosis of stroke patients. (sciencegate.app)
SUF pretreatment effectively improved the neurological function and cerebral infarction of MCAO rats, inhibited excessive inflammation in rats, protected the BBB, and inhibited cell apoptosis in brain tissue. (sciencegate.app)
Cerebral ischemia/reperfusion (I/R) injury is closely related to dysfunctional glucose metabolism. (sciencegate.app)
Celastrol is a bioactive compound that has been found to exhibit neuroprotective effects in cerebral ischemia, while whether it can protect against cerebral I/R injury by regulating glycolysis remains unclear. (sciencegate.app)
Therefore, we hypothesized that hearing loss after cerebral ischemia may be associated with changes to the synapse, gap junction, and sodium channel (NaC) proteins. (elsevierpure.com)
6. Xing B, Chen H, Zhang M, Zhao D, Jiang R, Liu X, Zhang S. Ischemic postconditioning inhibits apoptosis after focal cerebral ischemia/reperfusion injury in the rat. (ac.ir)
Ischemic postconditioning may not influence early brain injury induced by focal cerebral ischemia/reperfusion in rats. (ac.ir)
16. Wang Q, Zhang X, Ding Q, Hu B, Xie Y, Li X, Yang Q, Xiong L. Limb Remote Postconditioning Alleviates Cerebral Reperfusion Injury Through Reactive Oxygen Species-Mediated Inhibition of Delta Protein Kinase C in Rats. (ac.ir)
In former studies the expression of two different two-pore domain potassium (K 2P ) channels (TASK1, TREK1) were shown to ameliorate neuronal damage due to cerebral ischemia. (biomedcentral.com)
In C57Bl/6 (wildtype, WT), hcn2 +/+ and hcn2 -/- mice we used an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of HCN2 in stroke formation. (biomedcentral.com)
2004). We lately demonstrated that HNG protects against cerebral ischemia/reperfusion (I/R) damage by inhibiting apoptotic cell loss of life, reducing infarct quantity, and reducing neurological deficits in mice (Xu et al. (biomedigs.org)
Our earlier research proven that HNG exerts its neuroprotective results on cerebral ischemia damage by inhibiting the activation from the extracellular sign controlled kinase (ERK), indicating that HNG's protecting impact reaches least partly mediated from the tyrosine kinase Ras/MEK/ERK pathway (Xu et al. (biomedigs.org)
The neuroprotective part from the PI3K/Akt pathway in cerebral ischemia continues to be widely researched (Janelidze et. (biomedigs.org)
2002). In types of cerebral ischemia, Akt phosphorylation raises at 1 h and 4 h after I/R, but reduces considerably 24 h after reperfusion (Janelidze et al. (biomedigs.org)
Akt also exerts anti-apoptotic results by activating endothelial nitric oxide synthase (eNOS) (Brazil, Yang and Hemmings, 2004) Provided the neuroprotective part from the PI3K/Akt pathway in cerebral ischemia, we hypothesized that HN's neuroprotective impact requires the activation from the PI3K/Akt pathway after cerebral I/R damage. (biomedigs.org)
However, whether NRP-1 can repair mitochondrial structure and promote functional recovery after cerebral ischemia is still unknown. (biomedcentral.com)
Adeno-associated viral (AAV)-NRP-1 was stereotaxically inoculated into the cortex and ipsilateral striatum posterior of adult male Sprague-Dawley (SD) rats before a 90-min transient middle cerebral artery occlusion (tMCAO) and subsequent reperfusion. (biomedcentral.com)
Both in vitro and in vivo models of cerebral ischemia/reperfusion (I/R) injury presented a sharp increase in NRP-1 expression. (biomedcentral.com)
Therefore, promoting the mitochondrial structural repair and functional recovery is the crucial for the amelioration of the neurological damage after cerebral ischemia. (biomedcentral.com)
The contents of inflammasome proteins were gradually increased after cerebral ischemia/reperfusion (I/R). EA stimulus attenuated NLRP3 inflammasome mediated inflammatory reaction and regulated the balance between proinflammatory factors and anti-inflammatory cytokines. (biomedcentral.com)
2012 ). Our team has proposed a new approach of electroacupuncture (EA) neuroprotection for the prevention of cerebral ischemia injury. (biomedcentral.com)
Our previous studies have reported that EA could relieve neurological disorders, reduce infarct volumes after focal cerebral ischemia (Wang et al. (biomedcentral.com)
As an integrated platform for triggering inflammation, inflammasome contributes to the pathogenesis of initiating innate immune response after cerebral ischemia/reperfusion (I/R)(Ismael et al. (biomedcentral.com)
Ischemic stroke is sudden neurologic deficits that result from focal cerebral ischemia associated with permanent brain infarction (eg, positive results on diffusion-weighted MRI). (msdmanuals.com)

Results Coronary arterial ischemia/reperfusion depressed cardiac microcirculation, induced ST-segment elevation and increased infarct size in non-PTP and PTP rats. (ntnu.edu.tw)
Various concentrations of SUF, especially 5, 10 and 25 μg/kg of SUF, all alleviated the infarct size, neurological function and brain edema of MCAO rats. (sciencegate.app)
SUF also inhibited caspase3 and Bax rats and promoted Bcl2 in MCAO rats, thus inhibiting cell apoptosis. (sciencegate.app)
In this study, we investigated that if CDP-choline has protective effects against long-term myocardial ischemia-reperfursion injury in rats.Long term ischemia-reperfusion was produced in anaesthetized rats by ligature of the left main coronary artery for 30 minutes followed by reperfusion period for the next 180 minutes. (uludag.edu.tr)
Adult rats were subjected to myocardial ischemia/reperfusion (I/R) injury with or without ischemic preconditioning (IPC), and the level of miR‑133b‑5p in myocardium was measured. (spandidos-publications.com)
Approach and Results - Rats underwent 30-minute ischemia per 24-hour reperfusion. (utmb.edu)
Thirty Wistar rats were selected and divided into three groups (n = 10): acute ischemia-reperfusion (I/R) group, acute ischemia-reperfusion and treated with atorvastatin group and sham-operated group. (ac.ir)
Pretreating the rats with simvastatin 18 hour prior to the induction of ischemiareperfusion has been shown to reduce cardiac dysfunction and improve coronary flow [ 7 ]. (ac.ir)
2. Ren C, Yan Z, Wei D, Gao X, Chen X, Zhao H. Limb remote ischemic postconditioning protects against focal ischemia in rats. (ac.ir)
Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats. (ac.ir)
10. Allahtavakoli M, Jarrott B. Sigma-1 receptor ligand PRE-084 reduced infarct volume, neurological deficits, pro-inflammatory cytokines and enhanced anti-inflammatory cytokines after embolic stroke in rats. (ac.ir)
13. Zhang W, Miao Y, Zhou S, Jiang J, Luo Q, Qiu Y. Neuroprotective effects of ischemic postconditioning on global brain ischemia in rats through upregulation of hippocampal glutamine synthetase. (ac.ir)
The accumulation of cardiac lactate was attenuated by PLCA during myocardial I/R, and infarct size was smaller in rats treated with PLCA (1 mg/kg) than in those treated with caffeic acid (1 mg/kg). (biomedcentral.com)

Thus, inhibition of oxidative stress and myocardial apoptosis is beneficial in the treatment of myocardial I/R injury. (spandidos-publications.com)
The cardioprotective effect of CLU4A inhibition was detected by monitoring the cell viability, cell apoptosis, and LDH activity in vitro and in vivo , and examining the infarct size and cardiac function in vivo . (engreen.com.cn)
Inhibition of CLU4A improved the cell viability, restrained the cell apoptosis, and suppressed LDH activity in vitro . (engreen.com.cn)
Inhibition of Fas expression prevents I/R induced apoptosis. (ac.ir)
Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. (ac.ir)
In mice knock down or inhibition of specific platelets proteins like PAR-4, GPVI or P-selectin leads to reduced infarct size and reduced inflammation in the acute phase after I/R injury. (isth.org)
These protective effects may be associated with the inhibition of apoptosis and inflammation, as reflected by less TUNEL-positive cells and lower levels of serum proinflammatory cytokines (Interleukin-1β, Interleukin-6, tumor necrosis factor-α) and cardiac troponin I in the N-CM group compared with the vehicle group. (researchsquare.com)

This coupled comorbidity of pathological ischemia and therapeutic reinjury of infarcted myocardium, namely, myocardial ischemia-reperfusion injury (MIRI), is particularly refractory to treatment [ 4 , 5 ]. (hindawi.com)
Restoration of blood supply, termed reperfusion, has been used to treat ischemic myocardium and prevent further tissue damage. (spandidos-publications.com)
REPERFUSION of the myocardium after sustained ischemia induces myocardial cell necrosis and apoptosis, resulting in increased infarct size despite the restoration of coronary blood flow. (silverchair.com)
Both ischemic and reperfused rat myocardium can undergo apoptotic cell death, however the myocardium, which is subjected to ischemia followed by reperfusion, undergoes accelerated apoptosis [ 3 ]. (ac.ir)
Improved heart function was accompanied by reduced inflammation, including decreased cell-migration into the infarcted myocardium and improved cell survival in the infarct border zone as detected by reduced expression of pro-apoptotic proteins in the acute phase and reduced active caspase3 5 days after I/R. (isth.org)
Here we show, using large animal models of reperfused MI, that intramyocardial hemorrhage - the most damaging form of reperfusion injury (evident in nearly 40% of reperfused ST-elevation MI patients) - drives delayed infarct healing and is centrally responsible for continuous fatty degeneration of the infarcted myocardium contributing to adverse remodeling of the heart. (nature.com)

In conclusion, the present study demonstrated that SA inhibits the apoptosis of H9c2 cardiomyocytes following H/R injury via reduced activation of the p38MAPK and JNK signaling pathways. (spandidos-publications.com)
The results demonstrated that SA inhibited apoptosis signaling in H9c2 cardiomyocytes via downregulation of p38 mitogen-activated protein kinase (p38MAPK) and c-Jun N-terminal kinase (JNK) signaling pathways following hypoxia/reoxygenation (H/R) injury. (spandidos-publications.com)
HPC protected neonatal rat cardiomyocytes against H/R injury by increasing cell viability, while reducing LDH release and cell apoptosis. (spandidos-publications.com)
However, the knockdown of miR‑133b‑5p in the cardiomyocytes blocked HPC‑mediated cardioprotection as reflected by the aggravation of cell injury and apoptosis. (spandidos-publications.com)
Apoptosis of the cardiomyocytes was observed under electron microscopy and determined by optic microscopy with TUNEL (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling) staining. (ac.ir)
Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
Apoptosis of the cardiomyocytes has been demonstrated in animal models with coronary artery occlusion [ 1 ], and experimental evidence suggests that myocardial cells are able to undergo apoptosis during ischemia followed by reperfusion [ 2 ]. (ac.ir)
Our results show that platelets modulate inflammation and cell-survival after myocardial infarction indicating platelet interaction with inflammatory and endothelial cells and migration into the infarcted border zone to induce cell apoptosis of cardiomyocytes and / or inflammatory leukocyte. (isth.org)
Cardiomyocytes were isolated and subjected to 6 h hypoxia followed by 18 h reperfusion. (biomedcentral.com)
There is a growing body of evidence which demonstrates that following ACS, microRNAs might inhibit fibroblast proliferation and scarring, as well as harmful apoptosis of cardiomyocytes, and stimulate fibroblast reprogramming into induced cardiac progenitor cells. (archivesofmedicalscience.com)

We explored the acute effects of ticagrelor and clopidogrel on infarct size and potential long-term effects on heart function. (utmb.edu)
300 mg/kg per day) for 4 weeks starting 1 day after reperfusion or the combination (acute+chronic). (utmb.edu)
Therefore, we designed this study to see the influence of atorvastatin on cardiomyocyte apoptosis and Fas expression following acute I/R in vivo. (ac.ir)
Renal ischemia-reperfusion injury (IRI) is considered as a major cause of acute kidney injury. (frontiersin.org)
Acute kidney injury (AKI) can result from a variety of etiologies (e.g., ischemia, toxicity, and sepsis) and is characterized by high rates of morbidity and mortality. (biolifesas.org)
Prompt restoration of blood flow through the epicardial arteries (reperfusion) during the acute phase of MI (lasting hours to days: Fig. 1a ) has been a major advance and has reduced immediate death from acute MI with partial recovery of left ventricle function during the sub-acute phase of MI (lasting days to weeks: Fig. 1a ). (nature.com)
Acute MI may be either of the nonreperfusion type, in which case the obstruction to blood flow is permanent, or of the reperfusion type, in which the obstruction or lack of blood flow is long enough in duration (generally hours) but is reversed or restored after myocardial cell death occurs. (medscape.com)
Therefore, over the past several years, research has been directed to limit the brain lesions produced by acute ischemia (neuroprotection) and to increase the recovery, plasticity and neuroregenerative processes that complement rehabilitation and enhance the possibility of recovery and return to normal functions (neurorepair). (mdpi.com)
For example, research with animals found that supplementation with PQQ decreased the size of the area of the heart injured by acute coronary artery blockage . (lifeextension.com)

The PTP-induced protective effects on nicotinamide adenine dinucleotide phosphate oxidase gp91-mediated oxidative stress, ER stress, and apoptosis- and autophagy-related mechanisms were examined using Western blot and immunohistochemistry. (ntnu.edu.tw)
Infarct size measurement, cardiac troponin-I assays, oxidative stress analysis and histopathological analyzed. (edu.iq)

Short-term cardiac stress, induced by ischemia-reperfusion (I/R) injury resulted in impaired left ventricular (LV) recovery and increased infarct size in heterozygous Hmox1-deficient (Hmox1 +/− ) mice [ 55 ]. (springer.com)
CLU4A expression was measured after myocardial ischemia/reperfusion in mice and in H9C2 cells with hypoxia/reoxygenation treatment by q-PCR and western blotting. (engreen.com.cn)
Wild‐type C57BL/6J mice (male, 8-10 weeks old) were used and murine myocardial ischemia and reperfusion injury (IRI) model was conducted, cardiac function was evaluated by echocardiography. (edu.iq)
Ischemia- reperfusion injury was induced in wild-type mice (I/R group). (elsevierpure.com)
BBB disruption was confirmed by Evans blue staining and leakage of bovine serum albumin labeled with fluorescein isothiocyanate (BSA-FITC).Wefound that brain edema, infarct size, and permeability were increased in ischemic mice as compared with the sham-operated group. (elsevierpure.com)
Caspase-3, caspase-9, and TUNEL-positive cells were increased in I/R mice, indicating neuronal apoptosis. (elsevierpure.com)
In lpr mice, a naturally occurring mutant deficient in Fas, there is marked reduction in infarct size and abundance of apoptotic cardiac myocytes following ischemia and reperfusion that also signifies the importance of Fas pathway in ischemia-reperfusion injury [ 5 ]. (ac.ir)
Ischemia-induced cell depolarization: does the hyperpolarization-activated cation channel HCN2 affect the outcome after stroke in mice? (biomedcentral.com)
After 60 min of tMCAO induction in WT mice, we collected tissue samples at 6, 12, and 24 h after reperfusion. (biomedcentral.com)
Thrombocytopenia in mice leads to reduced infarct size and an improved left ventricular function 24 hours and 21 days after myocardial infarction. (isth.org)
Klier M, Ayhan A, Dannenberg L, Gorressen S, Polzin A, Elvers M. Role of Platelets in Processes of Myocardial Healing After Myocardial Ischemia and Reperfusion in Mice [abstract]. (isth.org)

As a whole, these outcomes claim that PI3K/Akt activation mediates HNG's protecting impact against hypoxia/ischemia reperfusion damage. (biomedigs.org)

2006). Finally, many research reported that HN inhibits apoptosis by binding intracellularly to Bax and Bet, thus obstructing apoptosis individually of receptors (Guo et al. (biomedigs.org)

The aim of the study is to investigate the effects of curcumin in attenuates myocardial ischemia and reperfusion-induced proinflammatory response through activation of the Nrf-2/HO-1 signaling pathway. (edu.iq)
Also, curcumin reduces cell apoptosis induced by myocardial IRI, curcumin reduces cell apoptosis induced by myocardial IRI and activates the Nrf-2/HO-1 signaling pathway during myocardial. (edu.iq)
It has been shown that the Fas pathway is functional in cardiac myocytes and plays a critical role in myocardial death due to ischemia-reperfusion in vivo [ 4 ]. (ac.ir)
7. Yuan Y, Guo Q, Ye Z, Pingping X, Wang N, Song Z. Ischemic postconditioning protects brain from ischemia/reperfusion injury by attenuating endoplasmic reticulum stress-induced apoptosis through PI3K-Akt pathway. (ac.ir)
The foam cells produce ceroids and destabilize the lysosomes and drive foam cell apoptosis, the remnants of which participate in fat deposition, with the released iron recycled to enter the pathway which perpetuates to continually support inflammation and growth of the fat depot. (nature.com)
2009 ) and regulate the Reperfusion Injury Salvage Kinase (RISK) signaling pathway (ERKε, PKC, GSK-3β, STAT3) via cannabinoid receptor 1 (CB1R)(Wang et al. (biomedcentral.com)

Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)

Additionally, machine reperfusion induces the production of ROS, which results in I/R injury to the heart. (gotomydoctor.com)
The uncoupling of glycolysis and glucose oxidation induces lactate accumulation during myocardial ischemia/reperfusion (I/R) injury. (biomedcentral.com)

However, while myocardial reperfusion is well established, the process itself can trigger myocardial reperfusion injury by causing further cardiomyocyte death through multiple pathophysiological mechanisms [ 3 - 5 ]. (hindawi.com)
Upregulation of Fas expression in myocardial ischemia-reperfusion can induce cardiomyocyte apoptosis, and atorvastatin can significantly inhibit cardiomyocyte apoptosis by inhibiting Fas expression. (ac.ir)
In this review, we focus on the role of cardiomyocyte-derived and cardiac fibroblast-derived microRNAs that are involved in the regulation of genes associated with cardiomyocyte and fibroblast function and in atherosclerosis-related cardiac ischemia. (archivesofmedicalscience.com)

Facilitation of glucose utilization contributes to the protective effect of AKT signaling to reduce infarct size and improve myocardial function in a heart subjected to I/R [ 15 ]. (biomedcentral.com)

Left main coronary artery occlusion generally results in a large anterolateral infarct, whereas occlusion of the left anterior descending coronary artery causes necrosis limited to the anterior wall. (medscape.com)
In hearts with a right coronary dominance (with the right artery supplying the posterior descending branch), a right coronary artery occlusion causes a posterior (inferior) infarct. (medscape.com)

All of these factors are known to result in myocardial apoptosis(5) and the acceleration of allograft rejection or chronic allograft dysfunction. (researchsquare.com)

While effective early reperfusion of the criminal coronary artery after a confirmed AMI is the typical treatment at present, collateral myocardial ischemia-reperfusion injury (MIRI) and pertinent cardioprotection are still challenging to address and have inadequately understood mechanisms. (hindawi.com)
We measured the cardiac O 2 - amount in vivo in response to left anterior descending coronary artery ligation for 2 hours and reperfusion for 3 hours. (ntnu.edu.tw)
Reperfusion after cardiac ischemia increases cell death and infarct size (IS), called myocardial ischemia/reperfusion (I/R) injury, which is the main cause of myocardial injury during the cardiac surgery particularly in coronary artery bypass graft surgery ( 1 , 2 ). (spandidos-publications.com)

Although, CDP-choline treatment did not significantly alter the blood levels of any parameter (ADMA, M30, M65, homocysteine, serum lipid profile).Results of this study show that CDP-choline exerts cardioprotective effects in long term myocardial ischemia-reperfusion injury. (uludag.edu.tr)
Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (I/R) injury. (ac.ir)
PLCA at 1 μM and metformin at 30 μM exerted similar effects on the improvement of cell viability and the alleviation of cell apoptosis in NRVM after H/R. PLCA promoted p-AMPK, p-AKT, and GLUT4 upregulation to induce a cardioprotective effect in both cell and animal model. (biomedcentral.com)

The underlying mechanisms behind myocardial I/R injury are associated with a number of factors, including substantial free radical production, intracellular calcium overload, increased inflammation, myocardial necrosis and apoptosis ( 6 ). (spandidos-publications.com)
In a word, our study showed that interfering with LncRNA AK139328 can reduce cell inflammation and apoptosis in CIRI. (sciencegate.app)
In contrast, non-hemorrhagic MIs are not iron-rich and do not result in prolonged inflammation or promote fat deposition, which stabilizes the infarct zone leading to stable functional remodeling in the chronic phase of infarction. (nature.com)

Fas/APO-1/CD95, member of the tumor necrosis factor (TNF) receptor superfamily, is a widely expressed cell surface receptor that can initiate apoptosis when activated by its ligand (FasL). (ac.ir)
In contrast, concentric subendocardial necrosis may result from global ischemia and reperfusion in cases of prolonged cardiac arrest with resuscitation. (medscape.com)
The anatomic variation due to microscopic collateral circulation, which is not evident at autopsy, plays a large factor in the size of necrosis and distribution. (medscape.com)

We tested the hypothesis that 8-Br is also protective under clinically relevant conditions (regional ischaemia) when applied either before ischemia or at the beginning of reperfusion, and this effect is associated with the mitochondrial permeability transition pore (MPTP). (mdpi.com)
Ischemia/reperfusion enhanced the cardiac O 2 - levels by enhanced nicotinamide adenine dinucleotide phosphate oxidase gp91 expression, cytosolic cytochrome C release, and decreased mitochondrial Bcl-2 expression. (ntnu.edu.tw)
Intracellular mechanisms underlying this so-called reperfusion injury presumably include increased levels of reactive oxygen species, Ca 2+ overload, rapid restoration of physiologic pH, and inflammatory processes resulting in opening of the mitochondrial permeability transition pore (mPTP). (silverchair.com)

Consistently, knockdown of CLU4A reduced the myocardial infarct size and improved cardiac function in vivo . (engreen.com.cn)

We suggest PTP might efficiently diminish cardiac ischemia/reperfusion-induced apoptosis and autophagy injury. (ntnu.edu.tw)
Cardiac injury activated ER stress-78-kDa glucose-regulated protein expression, increased the Bax/Bcl-2 ratio, cleaved caspase 3 expression and poly-(ADP-ribose)-polymerase fragments, leading to apoptosis formation, and promoted LC3-II expression, resulting in autophagy formation. (ntnu.edu.tw)
In some studies, CBD may coordinate autophagy, apoptosis, and the translocation of Beclin-1. (healthneu.com)

Conclusions PTP significantly reduced cardiac ischemia/reperfusion injury by upregulating antioxidant, antiapoptotic, and antiautophagic mechanisms. (ntnu.edu.tw)
End of the experiments we collected blood samples for the measurement of endothelial dysfunction parameter asymmetric dimethylarginine (ADMA), apoptosis parameters M30 and M65, cardiac risk factors homocysteine and serum lipid profile.CDP-choline treatment significantly attenuated the size of infarct area induced by long term ischemia-reperfusion versus saline group. (uludag.edu.tr)
Fas expression was significantly higher in the ischemia-reperfusion group as compared to sham-operated group, but was decreased significantly in atorvastatin treated group as compared with I/R group. (ac.ir)

9. Allahtavakoli M, Moloudi R, Arababadi MK, Shamsizadeh A, Javanmardi K. Delayed post ischemic treatment with Rosiglitazone attenuates infarct volume, neurological deficits and neutrophilia after embolic stroke in rat. (ac.ir)
The production of antioxidant enzymes that scavenge free radicals in ischemic tissue is then impaired, thereby exacerbating the damage caused by these free radicals in the post ischemic reperfusion tissue. (frontiersin.org)

Brain ischemia is known to include neuronal cell death and persisting neurological deficits. (biomedcentral.com)

Delayed postconditionig initiates additive mechanism necessary for survival of selectively vulnerable neurons after transient ischemia in rat brain. (ac.ir)

Flow cytometry was used to detect cell apoptosis, and apoptosisrelated proteins bcl-2, Bax, cleaved-caspase3 and cleaved PARP-1 were detected by western blot. (sciencegate.app)
Apoptosis is a genetically programmed form of cell death that is mediated by the activation of the caspase cascade and results in the cleavage of protein substrates and oligonucleosomal fragmentation of DNA. (ac.ir)
It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
Generally, neurotoxicity can be mediated by ionic imbalances that contribute to apoptosis (programmed cell death). (biomedcentral.com)
Cell apoptosis occurs, such as by activation of caspase-3 activity, and finally leads to myocardial infarction [ 1 ]. (biomedcentral.com)
Specifically, we show that the fatty degeneration of the hemorrhagic MI zone stems from iron-induced macrophage activation, lipid peroxidation, foam cell formation, ceroid production, foam cell apoptosis and iron recycling. (nature.com)
After 60 min of OGD and 24 h reperfusion, cell viability reduced to 52.9 0.93% from the control. (biomedigs.org)
Cell BMS-790052 viability was evaluated with the MTS assay at 24 h of reperfusion. (biomedigs.org)
2018 ). NLRP3 inflammasome is composed of NLRP3 (nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) pyrin domain-containing 3), ASC (apoptosis-associated speck-like protein containing a caspase recruitment domain) and procaspase-1, subsequently amplifying the production and secretion of proinflammatory cytokines, apoptotic and pyroptotic cell deaths(Zhong et al. (biomedcentral.com)
Promoting tumor cell death from apoptosis . (lifeextension.com)

The infarct size, neurological deficit score, TUNEL staining and the expression of proinflammatory factors or anti-inflammatory cytokines were evaluated at 72 h after reperfusion in the presence or absence of either α7nAChR antagonist (α-BGT) or agonist (PHA-543,613). (biomedcentral.com)

Also, previous studies showed that CDP-choline has protective effects against short-term myocardial ischemia-reperfusion injury. (uludag.edu.tr)

has been demonstrated to attenuate renal ischemia‑reperfusion (I/R) injury. (spandidos-publications.com)
Renal ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon in clinical settings. (frontiersin.org)

However, beta-adrenergic signaling displays a differential role in cardioprotection during reperfusion. (silverchair.com)

Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
Chien, CY , Chien, CT & Wang, SS 2014, ' Progressive thermopreconditioning attenuates rat cardiac ischemia/reperfusion injury by mitochondria-mediated antioxidant and antiapoptotic mechanisms ', Journal of Thoracic and Cardiovascular Surgery , 卷 148, 編號 2, 頁 705-713. (ntnu.edu.tw)

Finally, we clarified the apoptosis of brain tissue through the TUNEL staining and the detection of caspase3, Bcl2 and Bax. (sciencegate.app)
The microvascular and parenchymal organ damage induced upon ischemia tissue reperfusion is mainly attributed to the reactive oxygen-free radicals, and it has been demonstrated in many organs. (frontiersin.org)
The expression of NLRP3 inflammasome in the penumbral tissue following reperfusion was assessed by western blotting and immunoflourescent staining. (biomedcentral.com)

Cardiac function and injury were determined by microcirculation, electrocardiography, and infarct size. (ntnu.edu.tw)
Rapid recovery of the blocked coronary flow represents the most effective strategy to reduce the size of myocardial infarction and improve the cardiac function. (edu.iq)

Prior data show that 7-day pretreatment with ticagrelor limits infarct size. (utmb.edu)

Anatomy27

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