• However, the combined effect of prophylactic zinc administration and therapeutic taurine treatment on intrauterine ischemia- (IUI-) induced cerebral damage remains unknown. (hindawi.com)
  • These results collectively indicate the chronicity of oxidative stress and an inadequate antioxidant response after a cerebral hypoxia-ischemia event and have motivated the development of preventive and therapeutic approaches against oxidative stress. (hindawi.com)
  • Global cerebral ischemia followed by reperfusion, which leads to extensive neuronal damage, particularly the neurons in the hippocampal CA1 region. (springer.com)
  • Apoptosis is one of the major mechanisms that lead to neuronal death after cerebral ischemia and reperfusion. (springer.com)
  • The neuroprotective effects of remifentanil preconditioning against cerebral ischemia/reperfusion injury have been recently reported. (springer.com)
  • Here we investigated whether remifentanil postconditioning exerts neuroprotective effects against global cerebral ischemia/reperfusion injury in rats and its potential mechanisms. (springer.com)
  • Global cerebral ischemia was performed via 10 min of four-vessel occlusion. (springer.com)
  • We found remifentanil postconditioning markedly improved the spatial learning and memory as well as attenuated neuronal apoptosis in hippocampus caused by cerebral ischemia/reperfusion injury. (springer.com)
  • The results suggest that remifentanil postconditioning exhibits neuroprotective effects against global cerebral ischemia/reperfusion injury in rats, and its mechanisms might involve inhibition of neuronal apoptosis through the PI3K pathway. (springer.com)
  • Liang HW, Qiu SF, Shen J et al (2008) Genistein attenuates oxidative stress and neuronal damage following transient global cerebral ischemia in rat hippocampus. (springer.com)
  • Wang JY, Shen J, Gao Q et al (2008) Ischemic postconditioning protects against global cerebral ischemia/reperfusion-induced injury in rats. (springer.com)
  • Jeong S, Kim SJ, Jeong C et al (2012) Neuroprotective effects of remifentanil against transient focal cerebral ischemia in rats. (springer.com)
  • Upregulation of HIF-1 expression may play a neuroprotective role in animal models of focal cerebral ischemia ( 6 ). (spandidos-publications.com)
  • However, whether NRP-1 can repair mitochondrial structure and promote functional recovery after cerebral ischemia is still unknown. (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)
  • The expression of AAV-NRP-1 markedly ameliorated the cerebral I/R-induced damage to the motor function and restored the mitochondrial morphology. (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)
  • To understand its neuroprotective effect in vitro, GM-CSF was administered to a glutamate-induced excitotoxicity neuronal injury cell culture model that mimics the pathophysiology of focal hypoxic cerebral injury. (elsevierpure.com)
  • In the animal study, the authors prepared a rat focal cerebral ischemia model by occluding the unilateral middle cerebral artery. (elsevierpure.com)
  • Furthermore, in vivo administration of GM-CSF at 60 μg/kg body weight daily for 5 consecutive days beginning immediately after injury decreased infarction volume, altered the expression of several apoptosis-related genes (Bcl-2, Bax, caspase 3, and p53), and improved locomotor behavior in the focal cerebral ischemia model. (elsevierpure.com)
  • The study is the first to report on the neuroprotective effect of GCSF in vivo and showed that it improved neurological deficits that occur in the first few days following cerebral ischemia. (sciencedaily.com)
  • Results showed that GCSF improved neurological deficits that occur in the first few days following cerebral ischemia and improved long-term behavioral outcomes while also stimulating a neural progenitor recovery response. (sciencedaily.com)
  • Although the anti-apoptotic activity of GCSF is reported in global cerebral ischemia, this mechanism has not been fully explored. (sciencedaily.com)
  • Excitotoxic production of ROS elevates death-associated protein kinase (DAPK) activity, which provokes neuronal apoptosis in cerebral ischemia and seizure models 8 . (nature.com)
  • In this study, we compared the effect of gene deletion of PARP-1 and PARP-2, enzymes activated by DNA oxidative damage, in male mice subjected to 2 h of focal cerebral ischemia. (johnshopkins.edu)
  • We conclude that PARP-2 contributes substantially to nuclear translocation of AIF and infarct size after transient focal cerebral ischemia in male mice, but that protection is disproportionate to the attenuation of overall PARP activity. (johnshopkins.edu)
  • 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)
  • Any condition that increases intracranial pressure (ICP) may decrease cerebral perfusion pressure, resulting in secondary brain ischemia. (msdmanuals.com)
  • It was previously demonstrated that targeting of a Na + -Ca 2+ exchanger by miR-132 was able to prevent apoptosis of cardiomyocytes under hypoxic conditions ( 11 ). (spandidos-publications.com)
  • Apoptosis in both hypoxic and H 2 O 2 -treated cardiomyocytes were markedly reduced and cell viability was increased by miR-195 inhibitor. (ijbs.com)
  • Up-regulation of miR-195 in ischemic cardiomyocytes promotes ischemic apoptosis by targeting Bcl-2. (ijbs.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)
  • 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)
  • Effective pharmaceutical interventions for cisplatin-induced acute kidney injury (Cis-AKI) are currently lacking. (bvsalud.org)
  • Compared with wild-type littermates, these knockout mice were markedly more sensitive to cisplatin-induced acute kidney injury as indicated by renal functional loss, tissue damage, and apoptosis. (elsevierpure.com)
  • Yuan Y, Guo Q, Ye Z et al (2011) Ischemic postconditioning protects brain from ischemia/reperfusion injury by attenuating endoplasmic reticulum stress-induced apoptosis through PI3K-Akt pathway. (springer.com)
  • 7. Adenoviral TMBIM6 vector attenuates ER-stress-induced apoptosis in a neonatal hypoxic-ischemic rat model. (llu.edu)
  • Ren C, Yan Z, Wei D et al (2009) Limb remote ischemic postconditioning protects against focal ischemia in rats. (springer.com)
  • Ding ZM, Wu B, Zhang WQ et al (2012) Neuroprotective Effects of Ischemic Preconditioning and Postconditioning on Global Brain Ischemia in Rats through the same effect on inhibition of apoptosis. (springer.com)
  • The results demonstrated that Vitexin pretreatment significantly reduced neuronal apoptosis, and inhibited caspase‑3 activity, apoptosis regulator BAX protein expression and malondialdehyde levels in sevoflurane‑induced newborn rats. (spandidos-publications.com)
  • Together, the results of the current study suggest that the protective effect of vitexin reduces sevoflurane‑induced neuronal apoptosis through HIF‑1α‑, VEGF‑ and p38‑associated signaling pathways in newborn rats. (spandidos-publications.com)
  • 17. Role of PPAR-β/δ/miR-17/TXNIP pathway in neuronal apoptosis after neonatal hypoxic-ischemic injury in rats. (llu.edu)
  • We found that Fgl2 gene silencing inhibits apoptosis and improves heart function of streptozotocin (STZ)-induced diabetes rats, the possible mechanism maybe that Fgl2 gene silencing reduces the tumour necrosis factor (TNF)±levels, decreases the expression of B-cell lymphoma-2 (bcl2), bcl-2-associated X (bax), toll-like receptors 4 (TLR4) and p38 mitogen-activated protein kinase (MAPK). (silverchair.com)
  • Hang P, Sun C, Guo J, Zhao J, Du Z. BDNF-mediates Down-regulation of MicroRNA-195 Inhibits Ischemic Cardiac Apoptosis in Rats. (ijbs.com)
  • Cardiac function and apoptosis were detected in MI rats intravenously injected with antagomiR-195. (ijbs.com)
  • 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)
  • This study aimed to investigate the molecular mechanisms of protective effects of curcumin against cisplatin-induced kidney inflammation and apoptosis in rats. (thieme-connect.com)
  • Conclusions These data indicate that curcumin has nephroprotective properties against cisplatin-induced kidney damage in rats and this effect is associated with its anti-inflammatory and anti-apoptosis profiles, in addition to its antioxidant. (thieme-connect.com)
  • Previous studies have demonstrated that curcumin at a dose of 100 mg/kg orally in mice and 60 mg/kg in rats reduced concentration of tumor necrosis factor (TNF)-α and inhibited oxidative stress in cisplatin-induced nephrotoxicity [ 7 ] [ 8 ]. (thieme-connect.com)
  • Hypoxic-ischemic encephalopathy (HIE) following intrauterine ischemia (IUI) is one of the leading causes of brain injury in neonates, and the effects can endure until adulthood [ 1 , 2 ]. (hindawi.com)
  • In neonatal hypoxia-ischemia, an increase in reactive oxygen species (ROS) is known to occur in the brain at 96 h after a hypoxic-ischemic episode, to which the antioxidant system responds by increasing the activity of superoxide dismutase (SOD) and catalase (CAT) at postnatal day (PND) 11, which decreases afterward [ 5 ]. (hindawi.com)
  • 14. Chemerin reverses neurological impairments and ameliorates neuronal apoptosis through ChemR23/CAMKK2/AMPK pathway in neonatal hypoxic-ischemic encephalopathy. (llu.edu)
  • The present study was performed to investigate the role of miR-195 and the interplay between BDNF and miR-195 in ischemic cardiomyocyte apoptosis. (ijbs.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)
  • Ischemic stroke is characterised by ischemia-reperfusion damage, which happens when blood flow is restored after a period of ischemia. (digiwire.co.in)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • MicroRNAs (miRNAs) function as posttranscriptional regulators of expression levels of other genes by several mechanisms. (wikipedia.org)
  • The present study aimed to investigate whether the protective effect of vitexin protects against sevoflurane-induced neuronal apoptosis and the underlying mechanisms of this protective effect. (spandidos-publications.com)
  • We aimed to determine the ameliorative impact of diacerein on renal ischemia/reperfusion injury (I/R) condition, exploring the underlying mechanisms. (bvsalud.org)
  • The present study aimed to investigate the roles of miR‑132 in myocardial ischaemia/reperfusion (I/R) injury and the underlying mechanisms. (spandidos-publications.com)
  • Excitotoxicity, a critical process in neurodegeneration, induces oxidative stress and neuronal death through mechanisms largely unknown. (nature.com)
  • Over the last few decades, it has been studied that the mechanisms of cisplatin-induced kidney damage are complex and involved numerous cellular and molecular processes including inflammation, apoptosis, accumulation of cisplatin in renal tubular cells via renal drug transporters, Ctr1 and OCT2, and involvement of mitogen-activated protein kinases (MAPK) pathways [ 3 ] [ 4 ]. (thieme-connect.com)
  • However, the molecular mechanisms behind the anti-inflammatory and anti-apoptotic effects of curcumin in the cisplatin-induced kidney damage have not been explored. (thieme-connect.com)
  • Therefore, in this study, we aimed to investigate the possible molecular mechanisms of anti-inflammatory and anti-apoptotic effects of curcumin in cisplatin-induced kidney damage. (thieme-connect.com)
  • Fibrinogen-like protein 2 (Fgl2) is involved in apoptosis, angiogenesis and inflammatory response. (silverchair.com)
  • Researchers discovered that excessive induction of Fgl2 under certain medical conditions (e.g., pathogen invasion) could trigger complement activation, inflammatory response, cellular apoptosis and immune dysfunctions. (silverchair.com)
  • Furthermore, gene-expression levels of proinflammatory cytokines in the transplanted graft, including interleukin-6 (P =.04) and macrophage inflammatory protein 2 (P =.03) were significantly decreased in the DN group. (elsevierpure.com)
  • Moreover, upregulation in the expression of the inflammatory genes (TLR4, Myd88, and NLRP3), and overexpression of the pro-inflammatory cytokines (IL-1β), apoptotic (caspase-3) and pyroptotic (caspase-1) markers were observed in I/R-experienced animals. (bvsalud.org)
  • Nrf2 has anti-inflammatory and neuroprotective effects through boosting gene expression of anti-oxidant components. (digiwire.co.in)
  • 3 days later, we study lung pathological, the levels of inflammatory factors, and cell apoptosis in the pulmonary tissue was detected by Tunel and cell apoptosis rate was calculated accordingly. (researchsquare.com)
  • Hypoxia was found to induce A498 cell invasion, migration, and the release of inflammatory cytokines, while repressing human solute carrier family 14 member 1 gene expression. (biomedcentral.com)
  • Overexpression of the solute carrier family 14 member 1 gene could abolish hypoxia-induced invasion, reduce the migration of A498 cells, inhibit the hypoxia-induced release of inflammatory cytokines, and arrest the cell cycle at the G1/S checkpoint. (biomedcentral.com)
  • HDE-induced lung inflammatory aggregates clearly present in the tissue from HDE only exposed animals were not visually detectable in the HDE/alcohol co-exposure group. (cdc.gov)
  • Additionally, alcohol inhibits the lipopolysaccharide (LPS)-induced inflammatory cytokine, interleukin-6 (IL-6), via the p38 ERK1/2 MAPK pathway [ 9 ]. (cdc.gov)
  • TREM-1 deletion significantly abrogated hyperactivation of the platelet inflammasome and dramatically reduced AKI, whereas ablation of the mitophagy receptor BNIP3L/Nix induced the accumulation of damaged mitochondria and hyperactivation of platelet inflammasomes in CLP mice. (bvsalud.org)
  • Our results indicate that PKD1 inactivation underlies excitotoxicity-induced neuronal death and suggest that PKD1 inactivation may be critical for the accumulation of oxidation-induced neuronal damage during aging and in neurodegenerative disorders. (nature.com)
  • Excessive oxidative damage to DNA leads to activation of poly(ADP-ribose) polymerase-1 (PARP-1), accumulation of PAR polymers, translocation of apoptosis-inducing factor (AIF) from mitochondria to the nucleus, and cell death. (johnshopkins.edu)
  • The ischemia-induced increase in nuclear AIF accumulation was largely suppressed in both knockout genotypes. (johnshopkins.edu)
  • HRS and HBO could all decrease the release of immflammatory cytokines in lung tissue, reduce accumulation of oxidative products and alleviate apoptosis of pulmoanry cells, and could produce good therapeutic effects on ALI induced by LPS. (researchsquare.com)
  • Elevated levels of solute carrier family 14 member 1 expression induced mitochondrial reactive oxygen species accumulation, diminished the intracellular adenosine triphosphate level, and destroyed both mitochondrial membrane potential integrity and mitochondrial morphology. (biomedcentral.com)
  • Abstract Oral squamous cell carcinoma (OSCC) is a malignant tumor triggered by the accumulation of multiple gene mutations in oral epithelial cells. (techscience.com)
  • Ischemia and reperfusion can cause serious brain damage in stroke or cardiac arrest. (benbest.com)
  • 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)
  • Numerous studies have documented that cardiomyocyte apoptosis occurs in border zone of infarct scars and in the remote zone of non-infarcted myocardium [ 2 - 4 ], which exacerbates the post-MI remodeling and aggravates cardiac dysfunction [ 5 ]. (ijbs.com)
  • Thus, successfully reversal of cardiomyocyte apoptosis during early stage of MI is crucial for repairing the injured heart and ameliorating cardiac function [ 8 ]. (ijbs.com)
  • 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)
  • 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)
  • Cardiac transplantation is currently the optimal treatment for DCM-induced resistant chronic heart failure in children. (medscape.com)
  • 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)
  • Our previous studies suggested that brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TrkB) axis inhibited cardiomyocyte apoptosis in myocardial infarction (MI). (ijbs.com)
  • Studies have also suggested that both acute substantial cardiomyocyte loss and chronic low levels of apoptosis contributed to the development of heart failure [ 6 , 7 ]. (ijbs.com)
  • 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)
  • 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)
  • RAS dysfunction can also be caused by focal ischemia (eg, certain upper brain stem infarcts), hemorrhage, or direct, mechanical disruption. (msdmanuals.com)
  • Charron C, Messier C, Plamondon H (2008) Neuroprotection and functional recovery conferred by administration of kappa- and delta 1-opioid agonists in a rat model of global ischemia. (springer.com)
  • Using a mouse model, researchers investigated the efficacy of GCSF beyond the typical four-hour thrombolytic therapy (tPA) clot-busting drug -- the gold standard to treat stroke for global ischemia. (sciencedaily.com)
  • Several lines of evidence suggest that apoptosis-inducing factor mitochondrion-associated protein (AIFm2), a p53 target gene, a redox-responsive protein that resides in mitochondria and plays a central role in the caspase-independent cell death pathway. (lsuhs.edu)
  • The results elucidate a mechanism wherein the solute carrier family 14 member 1 gene participates in the occurrence and development of hypoxia-induced renal cell carcinoma in a mitochondria-dependent manner. (biomedcentral.com)
  • BACKGROUND: It is widely acknowledged that cisplatin-induced nephrotoxicity hinders its efficacy during clinical therapy. (bvsalud.org)
  • 2. Rh-CSF1 Attenuates Oxidative Stress and Neuronal Apoptosis via the CSF1R/PLCG2/PKA/UCP2 Signaling Pathway in a Rat Model of Neonatal HIE. (llu.edu)
  • cGAS/STING Pathway Activation Contributes to Delayed Neurodegeneration in Neonatal Hypoxia-Ischemia Rat Model: Possible Involvement of LINE-1. (llu.edu)
  • 9. Recombinant Slit2 attenuates neuronal apoptosis via the Robo1-srGAP1 pathway in a rat model of neonatal HIE. (llu.edu)
  • 10. Ghrelin attenuates oxidative stress and neuronal apoptosis via GHSR-1α/AMPK/Sirt1/PGC-1α/UCP2 pathway in a rat model of neonatal HIE. (llu.edu)
  • A recent study showed the activation of your p53 p21 pathway acts as being a big mediator of cel lular senescence induced by CKII inhibition in HCT116 colon carcinoma cells. (hsp70inhibitor.com)
  • In particular, extracellular-regulated kinase (ERK) 1/2, one of the MAPK pathway is considered as an important mediator of signal transduction processes, namely cell survival, cell division, gene expression, and cell metabolism that plays role in injury, death, and inflammation of kidney tubular cells due to cisplatin administration [ 5 ]. (thieme-connect.com)
  • Cecal ligation puncture (CLP)/LPS-induced AKI Triggering receptor expressed on myeloid cells (TREM-1)-knockout mice models were established. (bvsalud.org)
  • Ischemia-induced cell depolarization: does the hyperpolarization-activated cation channel HCN2 affect the outcome after stroke in mice? (biomedcentral.com)
  • Proximal tubular cells isolated from the knockout mice were more sensitive to cisplatin-induced apoptosis than cells from wild-type mice. (elsevierpure.com)
  • In addition, the knockout mice were more sensitive to renal ischemia-reperfusion injury than their wild-type littermates. (elsevierpure.com)
  • Hypoxia inducible factor-1 (HIF-1) is an oxygen-sensitive transcriptional regulator that regulates more than 70 downstream target genes, including vascular endothelial growth factor, erythropoietin, glucose transporter and so on ( 5 ). (spandidos-publications.com)
  • Generally, the regulation of target genes by miRNAs occurs through binding with the 3′-untranslated region (UTR). (spandidos-publications.com)
  • MicroRNAs are small non-coding post-translational biomolecules which, when expressed, modify their target genes. (archivesofmedicalscience.com)
  • Several targets for miR-184 have been described, including that of mediators of neurological development, apoptosis and it has been suggested that miR-184 plays an essential role in development. (wikipedia.org)
  • Brain ischemia is known to include neuronal cell death and persisting neurological deficits. (biomedcentral.com)
  • Objective We hypothesized that administration of a homodimer of recombinant annexin V, diannexin, could shield phosphatidylserine on the endothelium, and inhibit leukocyte and platelet adhesion, thereby potentially reducing ischemia reperfusion injury (IRI) in lung transplantation. (elsevierpure.com)
  • All-trans-retinoic acid induces miR-184 expression in neuroblastoma cell line and ectopic miR-184 causes apoptosis. (wikipedia.org)
  • In recent years, the MAPK family has been found to be an important signal-regulating enzyme between cell surface receptors and determinants of gene expression ( 8 ). (spandidos-publications.com)
  • Proteolysis of PARP to its stable 85kDa fragment is an early marker of programmed cell death (apoptosis) and is mediated by the caspase CPP32 protein. (thermofisher.com)
  • Our study found that fibrinogen-like protein 2 (Fgl2) gene silencing activates angiopoietin/Tie system and induces myocardial microvascular endothelial Cells proliferation and cell migration, we also found that serum Fgl2 levels elevated in patients with acute coronary syndrome (ACS), these results are preliminary, but very meaningful [ 1 , 2 ]. (silverchair.com)
  • MicroRNAs (miRNAs) are small endogenous RNAs that are associated with tumourigenesis, cell proliferation and apoptosis ( 4 , 5 ). (spandidos-publications.com)
  • Treatment with GM-CSF significantly increased cell viability in a cell culture model of glutamate-induced neuronal injury. (elsevierpure.com)
  • Cell viability and apoptosis were detected by MTT assay and TdT-mediated dUTP nick end labeling (TUNEL) staining, respectively. (ijbs.com)
  • 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)
  • 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)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
  • HBO combined with HRS seems to have a synergistic effect on the decrease of cell apoptosis, and in the expression of immflammatory cytokines and the generation of related immflammatory products, the combined use of HBO and HRS showed a decreasing trend as compared with simple application. (researchsquare.com)
  • Sequential activation of caspases plays a central role in the execution-phase of cell apoptosis. (thermofisher.com)
  • Generally, neurotoxicity can be mediated by ionic imbalances that contribute to apoptosis (programmed cell death). (biomedcentral.com)
  • There are lots of reviews that cross-linking antibodies (Abs) certain to the floor of B-lymphoma cells can induce apoptosis and/or cell dying, particularly with anti-CD20 Abs. (ncbcs.org)
  • The purpose of this study was to investigate the role and mechanism of hypoxia-induced renal cell carcinoma and provide evidence-based medical proof for improvements to postoperative nursing of renal cell carcinoma patients. (biomedcentral.com)
  • Caspase-cleaved cytokeratin 18 in plasma (a marker of epithelial apoptosis) was significantly reduced in the DN group (P =.013). (elsevierpure.com)
  • 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)
  • Furthermore, it was revealed that treatment with vitexin induced hypoxia inducible factor 1α subunit (HIF‑1α) and vascular endothelial growth factor (VEGF) protein expression, and suppressed phosphorylated‑p38 MAP kinase (p38) protein expression in sevoflurane‑induced newborn rat. (spandidos-publications.com)
  • By Western blot, this antibody recognizes a 116 kDa protein which corresponds to PARP and the 85 kDa apoptosis-induced cleavage product of prICE and CPP32 from rat thymus extract. (thermofisher.com)
  • They confirmed the neuroprotection of GCSF gene therapy in the BCAO mouse stroke model by a decrease of dynamin-related protein (DRP1), a marker of mitochondrial stress, in the frontal and middle brain of the GCSF treated group. (sciencedaily.com)
  • In contrast to protein interaction networks, enriched gene ontology (GO) terms of AMI related genes were used to construct a gene ontology interaction (GOI) network, which can be used to simulate the functional interactions between differential expressed genes of disease. (frontiersin.org)
  • These studies will not only extend our understanding of the fundamental mechanism by which these protein adducts are regulated in the myocardium but will also provide a solid rationale towards the specific putative binding sites available on AIFm2 in regulating NADH oxidoreductase activity during I/R injury-induced mitochondrial oxidative stress. (lsuhs.edu)
  • Familial AD (FAD) cases are caused by autosomal dominant mutations in the genes for amyloid precursor protein (APP) and the presenilins (PS1 and PS2) ( Sisodia and St George-Hyslop, 2002 ). (jneurosci.org)
  • This gene encodes a protein which is a member of the cysteine-aspartic acid protease (caspase) family. (thermofisher.com)
  • Alternative splicing of this gene results in two transcript variants that encode the same protein. (thermofisher.com)
  • Although the specific mechanism involved in stroke recovery was not fully elucidated as it was not the primary focus of this study, administration of GM-CSF appeared to decrease the extent of neuronal apoptosis by modulating the expression of several apoptosis-related genes such as Bcl-2, Bax, caspase 3, and p53. (elsevierpure.com)
  • A highly toxic aldehyde formed by reactive oxygen species (ROS) is 4-hydroxy-2-nonenal (HNE) through lipid peroxidation following myocardial ischemia/reperfusion (I/R) injury. (lsuhs.edu)
  • 8. Viral-mediated gene delivery of TMBIM6 protects the neonatal brain via disruption of NPR-CYP complex coupled with upregulation of Nrf-2 post-HI. (llu.edu)
  • Although the etiology of Alzheimer's disease (AD) is not completely understood, the study of disease genes that cause AD has revealed important clues about the pathogenesis of this disorder. (jneurosci.org)
  • Inhibition of Fas expression prevents I/R induced apoptosis. (ac.ir)
  • Hence clearly proposing that inhibition of telomer ase is a prospective therapy system for inducing senes cence. (hsp70inhibitor.com)
  • In one from the studies, using non modest lung adenocar cinoma A549 cells, it was proven that right after therapy with DNA damaging anti tumor drugs like caffeine, cells grow to be permanently growth arrested as being a end result of so known as drug induced more hints premature senescence or SIPS. (hsp70inhibitor.com)
  • A senescence inducing effect of doxorubicin over the very same cells, in yet another examine, had a dual impact it stopped the proliferation in the vast majority from the cells and led to the look of proliferating aneu ploid cells. (hsp70inhibitor.com)
  • Induction of apoptosis by cross-linking antibodies certain to human B-lymphoma cells: expression of Annexin V binding websites on the antibody cap. (ncbcs.org)
  • Countering NADH production, calcium action on the mitochondrial permeability transition pores increases inner membrane permeability thereby reducing proton potential, causing the matrix to swell and ultimately releasing cytochrome c (an initiator of apoptosis). (benbest.com)
  • Ischemia/ reperfusion was found to affect renal function and induce histopathological alterations. (bvsalud.org)
  • Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (I/R) injury. (ac.ir)
  • Binding of the miRNA can hinder translation of mRNA by promoting degradation or inducing deadenylation. (wikipedia.org)
  • MicroRNAs regulate gene expression at the post-transcriptional level by binding to 3′- or less often to 5′-untranslated regions of target messenger RNAs (mRNAs), which in consequence leads to inhibited translation and/or induces degradation of targeted mRNA [ 1 ]. (archivesofmedicalscience.com)
  • Here, we hypothesized that the absence of HCN2, an important functional counter player of TASK channels, affects neuronal survival during stroke-induced tissue damage. (biomedcentral.com)
  • The severity of these disabilities depends on the ischemia duration, damage expansion, and the affected brain region. (hindawi.com)
  • More than 15 million people worldwide suffer from stroke and our study provides new and important insights into GCSF induced protection as it relates to ER stress and mitochondrial stress activated apoptosis, " said Howard Prentice, Ph.D., corresponding author, a professor of biomedical sciences in FAU's Schmidt College of Medicine, and a member of FAU's I-BRAIN. (sciencedaily.com)
  • Therefore, it is of great significance finding an effective target to offset the I/R-induced neuronal damage. (biomedcentral.com)
  • SUMMARY: One of the reasons for acute kidney damage is renal ischemia. (bvsalud.org)
  • Ischaemia-reperfusion (I/R) injury is the most important and common cause of myocardial damage and subsequent heart failure worldwide ( 1 , 2 ). (spandidos-publications.com)
  • Even though various treatment strategies namely saline hydration and diuresis have been suggested for prevention of cisplatin-induced kidney damage, but its prevalence is still high. (thieme-connect.com)
  • In fact, the prevalence of cisplatin-induced kidney damage was 34% after fourth cycles and 52% after six cycles of cisplatin chemotherapy in adult cancer patients treated with cisplatin at a dose of ≥60 mg/m 2 at Dharmais National Cancer Hospital, Jakarta, Indonesia [ 6 ]. (thieme-connect.com)
  • In addition, remifentanil postconditioning enhanced the expression of anti-apoptotic gene Bcl-2 while suppressed the expression of pro-apoptotic gene Bax in hippocampal CA1 region. (springer.com)
  • They then examined the effects of GM-CSF administration on changes in infarct volume, apoptosis-related gene expression, and improvement in locomotor behavior. (elsevierpure.com)
  • MicroRNAs (miRNAs or miRs) refer to a group of small noncoding RNA molecules, typically 18~25 nucleotides in length, that function in RNA silencing and post-transcriptional regulation of gene expression [ 9 ]. (ijbs.com)
  • Subsequent analyses comprise behavioural tests and hcn2 gene expression assays. (biomedcentral.com)
  • Hcn2 gene expression levels in infarcted basal ganglia did not change after 6 h and 12 h. (biomedcentral.com)
  • Kinins (bradykinin and lys-bradykinin) are endogenous vasodilators and natriuretic peptides known best for their ability to antagonize angiotensin-induced vasoconstriction and sodium retention. (nature.com)