Effect of sodium hydrosulphide after acute compression injury of spinal cord

Abstract Background Early treatment of spinal cord white matter injury has been found beneficial. H2 S, a neurotransmitter is neuroprotective at lower doses. Purpose In the present study the effect of NaHS after clip compression injury of spinal cord white matter in vivo was studied. Methods The inj...

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Veröffentlicht in:Brain research 2013-08, Vol.1527, p.222-229
Hauptverfasser: Kesherwani, V, Nelson, K.S, Agrawal, S.K
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Sprache:eng
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Zusammenfassung:Abstract Background Early treatment of spinal cord white matter injury has been found beneficial. H2 S, a neurotransmitter is neuroprotective at lower doses. Purpose In the present study the effect of NaHS after clip compression injury of spinal cord white matter in vivo was studied. Methods The injury was induced in 8–10 weeks old Wistar rats by exposing the spinal cord at T8–T10 level by laminectomy and applying 35 g clip for 1 min. A dose of 50 µM NaHS was given intraperitoneally after 1 h of injury. 0.5 mm Spinal cord tissues were collected 8 h after injury from both sides including epicenter and dorsal column was microdissected and used for further study. Results NaHS treatment decreases nitric oxide (NO) by 27% and lipid peroxide (LPO) by 18% as compared to injury, which are hallmark of attenuation in oxidative stress. Western blots shows significant changes in Myeloperoxidase (MPO) level went down by 10%. GSH contents increased 44% in treated group as compared to the injury group. NaHS treatment increased Nrf-2 expression 1.8 times. We found NaHS treatment reduced the GFAP expression 8%, there was no significant changes in NF-200 after treatment and no evident morphological changes with H and E staining. Conclusions With the above data we conclude that NaHS at 50 µM dose at 1 h after injury reduces the NO, LPO, GFAP and MPO level at injury site by increasing the expression of Nrf-2. We expect that a decrease in these parameters during acute phase of spinal cord injury would be helpful in neuroprotection and regeneration.
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2013.06.023