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PloS one, ISSN 1932-6203, 2013, Volume 8, Issue 2, p. e55839
Background: Ischemic brain injury is associated with neuroinflammatory response, which essentially involves glial activation and neutrophil infiltration... 
PROTEIN | PHOSPHORYLATION | NICOTIFLORIN | NITRIC-OXIDE SYNTHASE | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | CEREBRAL-ARTERY OCCLUSION | ISCHEMIA | FLAVONOIDS | DAMAGE | INFILTRATION | Neuroprotective Agents - therapeutic use | Cerebral Infarction - drug therapy | Inflammation - pathology | Microglia - metabolism | Brain Injuries - drug therapy | Astrocytes - pathology | Kaempferols - therapeutic use | Male | NF-kappa B - metabolism | Stroke - pathology | Neuroprotective Agents - pharmacology | Inflammation - drug therapy | Inflammation Mediators - metabolism | Microglia - pathology | Infarction, Middle Cerebral Artery - drug therapy | STAT3 Transcription Factor - metabolism | Cerebral Infarction - pathology | Astrocytes - drug effects | NF-kappa B - antagonists & inhibitors | Microglia - drug effects | Kaempferols - chemistry | Monosaccharides - therapeutic use | Axons - drug effects | Rats | Stroke - drug therapy | Infarction, Middle Cerebral Artery - pathology | Rats, Sprague-Dawley | Stroke - metabolism | Animals | Axons - pathology | Monosaccharides - pharmacology | Kaempferols - pharmacology | Brain Injuries - pathology | Monosaccharides - chemistry | Astrocytes - metabolism | Brain | Transcription factors | Traumatic brain injury | Neuronal-glial interactions | Metastases | Proteins | Cell activation | Chinese medicine | Ischemia | Education | Cell adhesion | Inhibition | Alzheimer's disease | NF-κB protein | Intercellular adhesion molecule 1 | Neurological diseases | Flavonoids | Injury prevention | Nitric oxide | Pharmacy | Brain damage | Infiltration | Occlusion | Neuroprotection | Neurosciences | Phosphorylation | Drug delivery systems | Laboratories | Interleukin | Science | Activation | Kinases | Head injuries | Reperfusion | Cerebral blood flow | Rodents | Glycosides | Extracellular matrix | Tumor necrosis factor-TNF | Peroxidase | Metalloproteinase | Edema | Stroke | Kaempferol | Glial fibrillary acidic protein | Pharmacology | Inflammation | Amyloid precursor protein | Immunoreactivity | Brain injury
Journal Article
PloS one, ISSN 1932-6203, 03/2014, Volume 9, Issue 3, p. e89450
...)-induced injury by inhibiting the cytokine activity of high mobility group box 1 (HMGB1). In the present study, the protective effects of GL against I/R injury, as well as the related molecular mechanisms, were investigated in rat brains. Methods... 
ISCHEMIA-REPERFUSION INJURY | STROKE | CELLS | LIVER-INJURY | CHROMATIN PROTEIN HMGB1 | POSTISCHEMIC BRAIN | MEDIATOR | MULTIDISCIPLINARY SCIENCES | IN-VIVO | MOBILITY GROUP BOX-1 | HMG-1 | Neuroprotective Agents - therapeutic use | Cerebral Infarction - drug therapy | Inflammation - pathology | Apoptosis - drug effects | Reperfusion Injury - drug therapy | JNK Mitogen-Activated Protein Kinases - metabolism | Male | Cerebral Infarction - complications | Reperfusion Injury - blood | Inflammation - complications | Brain Ischemia - blood | Glycyrrhizic Acid - pharmacology | Neuroprotective Agents - pharmacology | Infarction, Middle Cerebral Artery - complications | Inflammation - drug therapy | Cerebral Infarction - blood | HMGB1 Protein - metabolism | Infarction, Middle Cerebral Artery - drug therapy | Reperfusion Injury - complications | p38 Mitogen-Activated Protein Kinases - metabolism | HMGB1 Protein - antagonists & inhibitors | Cerebral Infarction - pathology | Brain Ischemia - complications | Reperfusion Injury - pathology | Antioxidants - pharmacology | Infarction, Middle Cerebral Artery - pathology | Rats, Sprague-Dawley | Infarction, Middle Cerebral Artery - blood | Glycyrrhizic Acid - therapeutic use | Animals | MAP Kinase Signaling System - drug effects | Brain Ischemia - drug therapy | Brain Ischemia - pathology | Oxidative Stress - drug effects | Oxidative stress | Brain | Chromosomal proteins | Cytokines | Ischemia | Inflammation | Enzyme-linked immunosorbent assay | Apoptosis | Occlusion | Cytochrome | Cerebral cortex | Kinases | Caspase-3 | HMGB1 protein | Western blotting | Interleukin 6 | Reperfusion | Cerebral blood flow | Rodents | Inhibition | Pretreatment | Glycyrrhizin | Rats | Caspase | JNK protein | Tumor necrosis factor-α | Nitric-oxide synthase | Neurological diseases | Polymerase chain reaction | Cytochrome c | Serum levels | Signaling | Injury prevention | Molecular modelling | Nitric oxide | Immunofluorescence
Journal Article
PloS one, ISSN 1932-6203, 2016, Volume 11, Issue 7, p. e0158810
Dapagliflozin, a new type of drug used to treat diabetes mellitus (DM), is a sodium/glucose cotransporter 2 (SGLT2) inhibitor... 
TUBULAR CELLS | HYPOXIA-INDUCIBLE FACTOR | APOPTOSIS | HIF | GLUCOSE | MULTIDISCIPLINARY SCIENCES | LIVER | GENE-EXPRESSION | HIF-1-ALPHA | ERK ACTIVATION | FAILURE | AMP-Activated Protein Kinases - metabolism | Apoptosis - drug effects | Reperfusion Injury - drug therapy | Diabetic Nephropathies - drug therapy | Male | Extracellular Signal-Regulated MAP Kinases - metabolism | Hypoxia-Inducible Factor 1 - metabolism | Dose-Response Relationship, Drug | Reperfusion Injury - metabolism | Kidney Diseases - metabolism | Cell Line | Cell Hypoxia - drug effects | Diabetic Nephropathies - pathology | Glucosides - pharmacology | Kidney Tubules, Proximal - pathology | Reperfusion Injury - pathology | Kidney Diseases - pathology | Diabetic Nephropathies - metabolism | bcl-2-Associated X Protein - metabolism | Kidney Diseases - drug therapy | Sodium-Glucose Transporter 2 - antagonists & inhibitors | Animals | Kidney Tubules, Proximal - metabolism | Benzhydryl Compounds - pharmacology | Mice | Complications and side effects | Ischemia | Dapagliflozin | Dosage and administration | Research | Drug therapy | Reperfusion injury | Oxidative stress | Animal models | Nephrology | Hypoxia-inducible factor 1 | Renal function | Transplants & implants | Bax protein | Liver | Kinases | AMP-activated protein kinase | Proteins | Reperfusion | Rodents | Attenuation | Physiology | Inhibition | Hypoxia-inducible factors | Damage assessment | Oxygen | Cell survival | AMP | Diabetes mellitus | Extracellular signal-regulated kinase | Gene expression | Survival | Medicine | Injury prevention | Albendazole | Inhibitors | Sodium | Hypoxia | Kidney diseases | Diabetes | Apoptosis
Journal Article
PloS one, ISSN 1932-6203, 2015, Volume 10, Issue 10, p. e0140025
We examined whether endoplasmic reticulum (ER) stress-induced autophagy provides cytoprotection from renal tubular epithelial cell injury due to oxidants... 
ACUTE KIDNEY INJURY | SIGNALING PATHWAYS | IN-VITRO | ACTIVATION | UNFOLDED PROTEIN RESPONSE | INHIBITION | EPITHELIAL-CELLS | MULTIDISCIPLINARY SCIENCES | PROXIMAL TUBULE | CYTOTOXICITY | CELL-DEATH | Hypoxia - drug therapy | Kidney - pathology | Reperfusion Injury - drug therapy | Male | Protective Agents - therapeutic use | Autophagy - drug effects | Hypoxia - metabolism | Kidney - metabolism | Caspases - metabolism | Adenosine Triphosphate - metabolism | Cytoprotection - drug effects | Renal Insufficiency - complications | Renal Insufficiency - drug therapy | Reperfusion Injury - complications | Reperfusion Injury - metabolism | Cell Line | Unfolded Protein Response - drug effects | Kidney - drug effects | Endoplasmic Reticulum Stress - drug effects | Reperfusion Injury - pathology | Heat-Shock Proteins - metabolism | Mice, Inbred C57BL | Hypoxia - complications | Renal Insufficiency - metabolism | Oxidants - adverse effects | Tunicamycin - therapeutic use | Animals | Hypoxia - pathology | Renal Insufficiency - pathology | Mice | Oxidative Stress - drug effects | Cell death | Reperfusion injury | Cell culture | Hydrogen peroxide | Renal function | Butyl hydroperoxide | Epithelial cells | Chloroquine | Oxidizing agents | Tunicamycin | Cytotoxicity | Activation | Kinases | Autophagy | Proteins | Cell activation | Reperfusion | Ischemia | Oxidants | Protein folding | Antimycin A | Physiology | Inhibition | Injuries | Pharmaceutical sciences | Stresses | Immunoglobulins | Cell survival | Mortality | Caspase | Histology | Yang, Cindy | Stress | Medicine | Cell injury | Hypoxia | Iridium | Endoplasmic reticulum | Phagocytosis | Clear cell-type renal cell carcinoma | Cancer | Apoptosis
Journal Article
Journal of translational medicine, ISSN 1479-5876, 2019, Volume 17, Issue 1, pp. 127 - 14
Background: The sodium-glucose cotransporter-2 (SGLT2) inhibitor canagliflozin has been shown to reduce major cardiovascular events in type 2 diabetic... 
Sodium-glucose cotransporter-2 inhibitor | Cardioprotection | Canagliflozin | Myocardial ischemia-reperfusion injury | MEDICINE, RESEARCH & EXPERIMENTAL | CARDIOVASCULAR OUTCOMES | SGLT2 INHIBITORS | PHOSPHORYLATION | KINASE | CARDIOMYOCYTES | HEART | PRESSURE | AMPK | ARTERY | Apoptosis - drug effects | Canagliflozin - pharmacology | Myocardial Reperfusion Injury - complications | Systole - drug effects | Male | Aldehydes - metabolism | Liver - physiopathology | Cardiotonic Agents - therapeutic use | Liver - drug effects | Canagliflozin - therapeutic use | Diastole - drug effects | Aorta - physiopathology | Myocardial Reperfusion Injury - drug therapy | Phosphorylation - drug effects | Kidney - physiopathology | Biomarkers - metabolism | Endothelium - pathology | Glycosuria - physiopathology | Kidney - drug effects | Aorta - drug effects | Ventricular Function, Left - drug effects | Cardiotonic Agents - pharmacology | Rats, Sprague-Dawley | Glycosuria - complications | Myocardial Reperfusion Injury - physiopathology | Endothelium - physiopathology | Aorta - pathology | Endothelium - drug effects | Animals | Signal Transduction - drug effects | Oxidative Stress - drug effects | Vasodilation - drug effects | Blood Glucose - metabolism | Myocardial Reperfusion Injury - prevention & control | Nitrosative Stress - drug effects | Heart failure | Diabetics | Rats as laboratory animals | Analysis | Clinical trials | Research | Drug therapy | Health aspects | Occlusion | Myocardial infarction | Heart | Oxidative stress | Phosphorylation | Drug delivery systems | Intravenous administration | Heart attacks | Bax protein | 4-Hydroxynonenal | Bcl-2 protein | AKT protein | Myocardial ischemia | mRNA | Size determination | Kinases | Vasodilation | Proteins | Reperfusion | Ischemia | Rodents | Calcium-binding protein | Aorta | Heart diseases | Injury analysis | Medical research | Adenosine monophosphate | AMP | Diabetes mellitus | Coronary artery | Gene expression | Nitric-oxide synthase | Endothelium | Sodium | Protein kinase | Adenosine kinase | Nitric oxide | Ventricle | Diabetes | Laboratory animals | Apoptosis | Myocardial ischemia–reperfusion injury | Sodium–glucose cotransporter-2 inhibitor
Journal Article
PloS one, ISSN 1932-6203, 2014, Volume 9, Issue 2, p. e88916
Acute traumatic spinal cord injury (SCI) is marked by the enhanced production of local cytokines and pro-inflammatory substances that induce gliosis and prevent reinnervation... 
FUNCTIONAL RECOVERY | BODY-WEIGHT | ISCHEMIA/REPERFUSION INJURY | PROGENITOR-CELLS | NEURAL STEM/PROGENITOR CELLS | MULTIDISCIPLINARY SCIENCES | IN-VIVO | PROLIFERATION | IMPROVES LOCOMOTOR | NF-KAPPA-B | HISTOLOGICAL OUTCOMES | Spinal Cord Injuries - drug therapy | Curcumin - therapeutic use | Recovery of Function - drug effects | Curcumin - pharmacology | Neural Stem Cells - drug effects | Body Weight - drug effects | Rats | Neural Stem Cells - cytology | Rats, Sprague-Dawley | Spinal Cord Injuries - pathology | Stem Cell Transplantation | Organ Size - drug effects | Animals | Muscle, Skeletal - drug effects | Muscle, Skeletal - physiopathology | Neural Stem Cells - transplantation | Female | Cell Proliferation - drug effects | Spinal Cord Injuries - physiopathology | Muscle, Skeletal - pathology | Spinal Cord Injuries - therapy | Cytokines | Transplantation | Stem cells | Cell proliferation | Brain | Therapy | Spinal cord | Body weight | Bladder | Recovery of function | Neurosurgery | Spinal cord injury | Soleus muscle | Recovery | Subventricular zone | Proteins | Blood-brain barrier | Ischemia | Rodents | Tumor necrosis factor-TNF | Curcumin | Growth factors | Injuries | NF-κB protein | Free radicals | Antiinflammatory agents | Weight gain measurement | Muscles | Inflammation | Body weight gain | Trauma | Gliosis | Correlation analysis | Neural stem cells | Reinnervation | Spinal cord injuries | Apoptosis
Journal Article
PloS one, ISSN 1932-6203, 09/2014, Volume 9, Issue 9, p. e108024
... in the myocardial ischemia-reperfusion injury [1]. In the process of inflammation, various cytokines are released, including tumor necrosis factor α (TNF-α), interleukin 6... 
ISCHEMIA-REPERFUSION INJURY | APOPTOSIS | TUMOR-NECROSIS-FACTOR | INFARCTION | MULTIDISCIPLINARY SCIENCES | MONOCLONAL-ANTIBODY | CHEMOKINE | INHIBITOR | ARTHRITIS | DAMAGE | FACTOR-ALPHA | Tumor Necrosis Factor-alpha - metabolism | Lactate Dehydrogenases - metabolism | Apoptosis - drug effects | Creatine Kinase, MB Form - metabolism | Tumor Necrosis Factor-alpha - blood | Ventricular Dysfunction - drug therapy | Male | Troponin I - blood | Inflammation - metabolism | Myocardial Reperfusion Injury - pathology | Etanercept | Inflammation - drug therapy | Myocardial Infarction - pathology | Immunoglobulin G - pharmacology | Myocardial Reperfusion Injury - drug therapy | Myocardial Reperfusion Injury - genetics | Neutrophil Infiltration - drug effects | Superoxide Dismutase - metabolism | Disease Models, Animal | Malondialdehyde - metabolism | Glutathione Peroxidase - metabolism | Rats | Toll-Like Receptor 4 - genetics | Receptors, Tumor Necrosis Factor - administration & dosage | Myocardial Infarction - metabolism | Immunoglobulin G - administration & dosage | Toll-Like Receptor 4 - metabolism | Myocardial Reperfusion Injury - physiopathology | Gene Expression Regulation - drug effects | Myocardial Reperfusion Injury - metabolism | Animals | Myocardial Infarction - drug therapy | Myocytes, Cardiac - drug effects | Creatine Kinase, MB Form - blood | Myocytes, Cardiac - metabolism | Oxidative Stress - drug effects | Troponin I - metabolism | Myocardial infarction | Bioengineering | Heart | Oxidative stress | Critical care | Superoxide dismutase | Myocardial ischemia | Arthritis | Antioxidants | Reperfusion | Ischemia | Rodents | Tumor necrosis factor-TNF | Peroxidase | Injuries | Glutathione | Creatinine | Glutathione peroxidase | Psoriasis | Cytokines | Neutrophils | Cardiomyocytes | Lactate dehydrogenase | Inflammation | Tumor necrosis factor-α | Gene expression | Malondialdehyde | L-Lactate dehydrogenase | Digital imaging | TNF inhibitors | Infarction | Lactic acid | Laboratory animals | Apoptosis
Journal Article
Brain research, ISSN 0006-8993, 12/2017, Volume 1677, pp. 118 - 128
•(−)-Phenserine reduced infarct volume in a rat MCAO model of ischemia/reperfusion injury... 
Glial fibrillary acidic protein (GFAP) | Metallopeptidase-9 (MMP-9) | Stroke | ERK-1/2 signaling pathway | Ischemia/reperfusion injury | Activated-caspase 3 | Brain-derived neurotrophic factor (BDNF) | Amyloid precursor protein (APP) | (−)-Phenserine | Middle cerebral artery occlusion (MCAO) | B-cell lymphoma 2 (Bcl-2) expression | FUNCTIONAL RECOVERY | NEUROTROPHIC FACTOR | FOCAL CEREBRAL-ISCHEMIA | AMYLOID PRECURSOR PROTEIN | NEUROSCIENCES | MATRIX METALLOPROTEINASES | MESSENGER-RNA | (-)-Phenserine | MATRIX-METALLOPROTEINASE-9 | BRAIN-BARRIER DISRUPTION | TRANSGENIC MICE | Neurons - pathology | Cell Hypoxia - physiology | Apoptosis - drug effects | Humans | Reperfusion Injury - drug therapy | Brain Ischemia - metabolism | Male | Dose-Response Relationship, Drug | Stroke - pathology | Neuroprotective Agents - pharmacology | Neurons - metabolism | Neurons - drug effects | Reperfusion Injury - metabolism | Cell Survival - physiology | Cell Survival - drug effects | Cell Hypoxia - drug effects | Physostigmine - analogs & derivatives | Reperfusion Injury - pathology | Rats | Stroke - drug therapy | Rats, Sprague-Dawley | Physostigmine - pharmacology | Glucose - deficiency | Stroke - metabolism | Animals | Cholinesterase Inhibitors - pharmacology | Brain Ischemia - drug therapy | Brain Ischemia - pathology | Cell Line, Tumor | Apoptosis - physiology | Brain | Neurons | Analysis | Injuries | Apoptosis | Stroke (Disease) | Amyloid beta-protein | Lymphomas | middle cerebral artery occlusion (MCAO) | brain-derived neurotrophic factor (BDNF) | metallopeptidase-9 (MMP-9) | activated-caspase 3 | reperfusion injury | stroke | amyloid precursor protein (APP) | glial fibrillary acidic protein (GFAP) | ischemia | ERK-1 | 2 signaling pathway
Journal Article