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1

Hydrogen gas reduces brain injury in a global cerebral ischemia model

100%
Ostrowski R. P., Mansell C., Zhang J. H.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
Transient global cerebral ischemia-reperfusion injury can occur during acute severe hypotensive states and in cardiac arrest that is followed by resuscitation. This transient reduction in perfusion causes an insult to selective hippocampal neuronal populations via an apoptotic mechanism. Hydrogen gas has a neuroprotective effect and could be used as a pharmacologic agent of beneficial effect. As such we set out in this study to describe the effect of the inhalation of 2.9% hydrogen enriched air following an ischemia-reperfusion injury. A 2-vessel occlusion model was used to induce global cerebral ischemia for 6 minutes while maintaining a hypotensive state with a mean arterial pressure of 30 mm Hg through reversible exsanguinations in male Sprague-Dawley rats (280–330 g). The study included three groups: global ischemia without treatment (GI, n=6), global ischemia with hydrogen (GI + H2, n=6 ) and sham surgery (Sham, n=6). Rats in the treatment group received 2.9% inhalational hydrogen for 1 hour starting 15 minutes following reperfusion. Neurobehavioral testing was performed on day one and T-maze testing prior to being euthanized on days 3 or 7. Treated rats demonstrated an improved outcomes in spontaneous alternations, seizure incidence and survivability. Quantitative Nissl histology and TUNEL of the CA-1 region of the hippocampus showed increased cell survival in the treatment group. We conclude that treatment with inhalational hydrogen following ischemia-reperfusion injury could be low cost method of decreasing the effects of neuronal cell death.
2

Effect of novel pentabromobenzylisothioureas on T98G human glioblastoma cell lines and SEGA-derived cultures

88%
Pucko E. B., Koronkiewicz M., Kazimierczuk Z., Ostrowski R. P., Matyja E.
Acta Neurobiologiae Experimentalis
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2013
|
tom 73
|
nr Suppl.1
Gliomas are the most common primary brain tumours characterized by infiltrative cell growth. The specific novelty inhibitors of constitutively active serine/threonine kinase (CK2), i.e. isothiourea derivatives induce apoptosis and affect proliferation in some human cancer cells. We examined the cytotoxic and proapoptotic effect of selected modified isothiourea derivatives – pentabromobenzylisothioureas (ZKKs) against T98G adult human glioblastoma cell lines and cultures derived from rare, low-grade pediatric brain tumour of a mixed glioneuronal lineage (subependymal giant cell astrocytoma – SEGA), and normal human cultured astrocytes. ZKK-3 and ZKK-2 appeared to be the most effective compounds that induce apoptosis and exhibit strong anti-proliferative effect on neoplastic astroglial cells determined by flow cytometry analysis and Multisizer3 Beckman Coulter. Treatment of T98G cell line and SEGAderived cell cultures with 50 µM ZKK-3 and ZKK-2 for 48 h resulted in apoptosis and inhibition of cell proliferation up to 60% and 50% respectively. These results might suggest the potential anti-tumour effect of selected ZKKs related with glioma-derived neoplasms.
3

Dual endothelin receptor antagonist reduces subcellular organelles damage in cerebral cortex neurons in experimental model of cardiac arrest

76%
Ostrowski R. P., Januszewski S., Kowalska Z., Kapuscinski A., Frontczak-Baniewicz M., Pucko E. B., Matyja E.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
In the present study we investigated the effect of dual endothelin receptor (ETR) antagonist bosentan on postischemic structural abnormalities of subcellular organelles in neurons of cerebral cortex and on endothelin binding sites in the brain after 10 min of cardiac arrest in male Wistar rats. After seven days, cortical neurons in bosentantreated animals revealed diminished morphological changes compared with non-treated rats, including less advanced nuclear pore formation, disaggregation of ribosomes, abnormalities of Golgi network and better preservation of long neurotubules. The analysis of 125I-endothelin-1 binding in brain documented a decrease in endothelin-1 maximum density of receptors (Bmax) and equilibrium dissociation constant (KD) up to 1 week in untreated animals. In bosentan-treated animals above values increased postischemically. In conclusion, the results indicate that bosentan works towards salvage of cytoskeleton and other organelles of cortical neurons after cardiac arrest through a modulation of ETR signaling.
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