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Tin chloride enhances parvalbumin-positive interneuron survival by modulating heme metabolism in a model of cerebral ischemia.

Authors: Li Volti, G  Zappala, A  Leggio, GM  Mazzola, C  Drago, F  La Delia, F  Serapide, MF  Pellitteri, R  Giannone, I  Spatuzza, M  Cicirata, V  Cicirata, F 
Citation: Li Volti G, etal., Neurosci Lett. 2011 Mar 29;492(1):33-8. doi: 10.1016/j.neulet.2011.01.048. Epub 2011 Jan 27.
Pubmed: (View Article at PubMed) PMID:21276833
DOI: Full-text: DOI:10.1016/j.neulet.2011.01.048

SnCl(2) has been reported to increase the expression of heme-oxygenase 1 (HO-1), a major antioxidant enzyme, and to decrease ischemic injury, in non-nervous tissues. This study examined the neuroprotective effect of SnCl(2) in the hippocampus of rats submitted to cerebral ischemia. SnCl(2) was administered 18 h before bilateral carotids obstruction. Changes in HO-1 expression and activity, heme content, inducible nitric oxide synthase (iNOS) expression and parvalbumin positive interneuron survival were studied. Thereafter both behavior and memory recovery were tested. The administration of SnCl(2) increased the expression of HO-1 protein and HO activity in the hippocampus and concomitantly decreased heme content at both mitochondrial and nuclear level. Furthermore, ischemized animals showed a strong increase in iNOS expression in the hippocampus, where a loss of parvalbumin positive interneurons also occurred. Pre-treatment with SnCl(2), decreased both iNOS expression in ischemized rats and increased cell survival. The beneficial effects of SnCl(2) were prevented by concomitant treatment with SnMP, a strong inhibitor of HO activity. SnCl(2) also caused an improvement in short term memory recovery. Our results showed that following SnCl(2) administration, HO-1 is strongly induced in the hippocampus and modulate iNOS expression, resulting in a strong neuroprotective effect.


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RGD Object Information
RGD ID: 10755576
Created: 2016-02-02
Species: All species
Last Modified: 2016-02-02
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.