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Protective effects of Phoenix dactylifera against oxidative stress and neuronal damage induced by global cerebral ischemia in rats
, Neeraj Vyawahare S., Prasad Thakurdesai A.
Published in
2013
Volume: 3
   
Issue: 2
Pages: 75 - 81
Abstract
Phoenix dactylifera (PD) has been claimed for its neuroprotective potential in the traditional system of medicine but has not yet been scientifically documented. Phytochemical reports of Phoenix dactylifera fruits have demonstrated the presence of polyphenols and flavonoids, which have already been documented to play major role in neuroprotection against various experimental models of cerebral ischemia/reperfusion. In the present study, we have investigated the neuroprotective as well as antioxidant properties of methanolic extract of Phoenix dactylifera fruits (MEPD) at 30, 100, 300 mg/kg p.o against global cerebral ischemia-induced oxidative stress and neuronal death. The global cerebral ischemia was induced by occlusion of bilateral common carotid arteries for 5 min followed by 24 h of reperfusion. Varied biochemical/enzymatic alterations, produced subsequent to the application bilateral common carotid artery occlusion (BCCAO) followed by reperfusion viz. increase in lipid peroxidation and decrease in glutathione, glutathione reductase, catalase, glutathione-S-transferase, glutathione peroxidase and superoxide dismutase, were markedly reversed and restored to near normal levels in the groups pre-treated with 15 days. The pretreatment also reversed the histopathological changes induced by global cerebral ischemia in CA1 hippocampal region. The protective action, exhibited by MEPD against global cerebral induced brain injury, suggests its therapeutic potential in cerebrovascular diseases (CVD) including stroke. These findings are important because the present treatment strategies for CVD are far from adequate and PD with wide usage is known to be a safe natural product. {\textcopyright} 2013 Elsevier Masson SAS.
About the journal
JournalBiomedicine and Aging Pathology
ISSN22105220
Open AccessNo