Novel application of amino-acid buffered solution for neuroprotection against ischemia/reperfusion injury
Autoři:
Jiun Hsu aff001; Chih-Hsien Wang aff002; Shu-Chien Huang aff002; Yung-Wei Chen aff001; Shengpin Yu aff001; Juey-Jen Hwang aff003; Jou-Wei Lin aff003; Ming-Chieh Ma aff004; Yih-Sharng Chen aff002
Působiště autorů:
Department of Cardiovascular Surgery, National Taiwan University Hospital Yunlin Branch, Yunlin, Taiwan
aff001; Department of Cardiovascular Surgery, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan
aff002; Department of Cardiovascular Medicine, National Taiwan University Hospital Yunlin Branch, Yunlin, Taiwan
aff003; School of Medicine, Fu Jen Catholic University, New Taipei, Taiwan
aff004
Vyšlo v časopise:
PLoS ONE 14(9)
Kategorie:
Research Article
prolekare.web.journal.doi_sk:
https://doi.org/10.1371/journal.pone.0221039
Souhrn
Ischemic neuron loss contributes to brain dysfunction in patients with cardiac arrest (CA). Histidine–tryptophan–ketoglutarate (HTK) solution is a preservative used during organ transplantation. We tested the potential of HTK to protect neurons from severe hypoxia (SH) following CA. We isolated rat primary cortical neurons and induced SH with or without HTK. Changes in caspase-3, hypoxia-inducible factor 1-alpha (HIF-1α), and nicotinamide adenine dinucleotide phosphate oxidase-4 (NOX4) expression were evaluated at different time points up to 72 h. Using a rat asphyxia model, we induced CA-mediated brain damage and then completed resuscitation. HTK or sterile saline was administered into the left carotid artery. Neurological deficit scoring and mortality were evaluated for 3 days. Then the rats were sacrificed for evaluation of NOX4 and H2O2 levels in blood and brain. In the in vitro study, HTK attenuated SH- and H2O2-mediated cytotoxicity in a volume- and time-dependent manner, associated with persistent HIF-1α expression and reductions in procaspase-3 activation and NOX4 expression. The inhibition of HIF-1α abrogated HTK’s effect on NOX4. In the in vivo study, neurological scores were significantly improved by HTK. H2O2 level, NOX4 activity, and NOX4 gene expression were all decreased in the brain specimens of HTK-treated rats. Our results suggest that HTK acts as an effective neuroprotective solution by maintaining elevated HIF-1α level, which was associated with inhibited procaspase-3 activation and decreased NOX4 expression.
Klíčová slova:
Biology and life sciences – Cell biology – Biochemistry – Physical sciences – Chemistry – Proteins – Neuroscience – Cellular types – Animal cells – Medicine and health sciences – Chemical compounds – Pathology and laboratory medicine – Amino acids – Organic compounds – Organic chemistry – Critical care and emergency medicine – Resuscitation – Diagnostic medicine – Signs and symptoms – Neurology – Vascular medicine – Cellular neuroscience – Neurons – Basic amino acids – Ischemia – Asphyxia – Brain damage – Cerebral ischemia – Hypoxia – Histidine
Zdroje
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