eISSN: 1896-9151
ISSN: 1734-1922
Archives of Medical Science
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SCImago Journal & Country Rank
2/2019
vol. 15
 
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abstract:
Experimental research

Neuroprotective effects of the new Na channel blocker rs100642 in global ischemic brain injury

Suat Kamisli
,
Cenk Basaran
,
Kadir Batcioglu
,
Mustafa Namık Oztanir
,
Mehmet Gul
,
Basri Satilmis
,
Ayse Burcin Uyumlu
,
Basak Kayhan
,
Metin Genc

Arch Med Sci 2019; 15, 2: 467–474
Online publish date: 2019/03/04
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Introduction
RS100642, a mexiletine analogue, is a novel sodium channel blocker with neuroprotective and antioxidant activities. The protectivity of RS100642, which has been shown against focal cerebral ischemia, was investigated in global cerebral ischemia in this study.

Material and methods
Global cerebral ischemia was induced for five minutes in adult male Wistar Albino rats via the 4-vessel occlusion method. Intravenous administration of 1 mg/kg RS100642 following reperfusion for 30 min (RS100642 group) was compared with a sham treatment group (ischemia group) and nonischemized group (control) histologically based on morphology and caspase-3 immunohistochemistry, and biochemically based both on measurement of oxidative stress including malondialdehyde (MDA) levels, superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) activities and on assessment of apoptosis including caspase-3 and -8 activities and tumor necrosis factor α (TNF-α) levels at the end of 6 h.

Results
While the RS100642 group had significantly lower MDA levels and higher SOD activities than the sham treatment group (p < 0.05), GPx and CAT activities of the RS100642 and sham treatment groups were similar (p > 0.05) and significantly lower than those of the controls (p < 0.05). Necrosis and caspase-3 activity and immunoreactivity in the RS100642 group were significantly lower than those in the sham treatment group (p < 0.05), while there was no significant difference between groups regarding caspase-8 and TNF-α (p > 0.05).

Conclusions
Na+ channel blockade by RS100642 has remarkable neuroprotective effects following global brain ischemia/reperfusion damage. Further research is required to determine the optimum dose and time of administration.

keywords:

brain injury, global cerebral ischemia, sodium channels, neuroprotection

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