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Pharmacol Res. 2007 Apr;55(4):335-42. Epub 2007 Jan 16.

FeTPPS protects against global cerebral ischemic-reperfusion injury in gerbils.

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1
Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Sector-67, S.A.S. Nagar, Punjab 160062, India. sssharma@niper.ac.in

Abstract

Neuronal damage following cerebral ischemia is mediated by various mechanisms, among which nitrosative stress plays an important role. Peroxynitrite, a powerful oxidant, contributes heavily to the neuronal damage in cerebral ischemic-reperfusion (IR) injury. In the present study, we have investigated the neuroprotective effects of a peroxynitrite decomposition catalyst, 5,10,15,20-tetrakis(4-sulfonatophenyl) porphyrinato iron(III) [FeTPPS] in global cerebral IR injury in gerbils. Neurological damage was significantly attenuated by FeTPPS treatment (1 and 3mgkg(-1), i.p.) as evident from reduction in neurological symptoms, hyperlocomotion, memory impairment and CA1 hippocampal neuronal damage in IR challenged gerbils. FeTPPS treatment also attenuated the increased malondialdehyde (MDA) levels and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) positive cells after cerebral IR injury. Results of this study demonstrates the neuroprotective activity of FeTPPS in global cerebral IR injury and its neuroprotective effects may be attributed to reduction in oxidative stress and DNA fragmentation.

PMID:
17292620
DOI:
10.1016/j.phrs.2007.01.002
[Indexed for MEDLINE]
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