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Abstract
Objective. The aim of this study was to investigate the possible neuroprotective and ameliorating effects of leptin treatment in hypoxic-ischemic injury induced neuronal cell death.
Methods. Experimental groups in the study were: sham-operated group, leptin treated hypoxia–ischemia group, and vehicle treated hypoxia–ischemia group. In hypoxia–ischemia group, left common carotid artery was ligated permanently on the seventh postnatal day. Two hours after the procedure, hypoxia (92% nitrogen and 8% oxygen) was applied for 2.5 h. Leptin treatment was injected (intraperitoneally; i.p.) as a single dose immediately after the hypoxia period. Neuronal cell death, neuronal density, and leptin levels were evaluated in both hemispheres 72 h after the hypoxic-ischemic insult.
Results. Compared with the hypoxic-ischemia group, the mean leptin levels were higher in the brains of the sham group for both hemispheres. The leptin treatment significantly diminished the number of ‘apoptotic cells’ in the hippocampal CA1, CA2, CA3, and gyrus dentatus regions in both hemispheres. Leptin treatment significantly preserved the number of neurons in both hemispheres, when compared with the vehicle treated group.
Conclusion. We conclude that leptin treatment improves neuronal density and decreases apoptosis in the newborn rat with hypoxic-ischemic brain injury.
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Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.