Pomegranate protective effect on experimental ischemia/reperfusion retinal injury in rats (histological and biochemical study)

Oxidative stress is one mechanism involved in the pathogenesis of ischemia/reperfusion (/R) retinal injury. The histological, biochemical, and functional changes associated with pomegranate (PMG) treatment prior to retinal I/R were analyzed using 40 adult male albino rats. Rats were divided into fou...

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Published in:Ultrastructural pathology 2017-09, Vol.41 (5), p.346-357
Main Authors: Hashem, Hala E., Abd El-Haleem, Manal R., Amer, Mona G., Bor'i, Ashraf
Format: Article
Language:English
Subjects:
Animals
Antioxidants - pharmacology
Apoptosis - drug effects
Electroretinography - methods
Male
Microscope
nuclear factor
Oxidative Stress - drug effects
pomegranate
Punicaceae - chemistry
Reperfusion Injury - pathology
retina
Retina - drug effects
Retina - injuries
Superoxide Dismutase - metabolism
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Summary:Oxidative stress is one mechanism involved in the pathogenesis of ischemia/reperfusion (/R) retinal injury. The histological, biochemical, and functional changes associated with pomegranate (PMG) treatment prior to retinal I/R were analyzed using 40 adult male albino rats. Rats were divided into four groups: Groups I and II (sham operated and received saline or PMG, respectively); Groups III and IV (I/R rat models with prior administration of saline or 250 mg/kg/day PMG, respectively). Electroretinogram (ERG) results were recorded and eye specimens were taken and processed for light and electron microscopic examinations and for assessment of oxidative status in retinal homogenate. I/R lead to degenerative changes in retinal layers with a significant reduction in nuclear factor erythroid 2-related factor 2 (Nrf2) immunoreactivity in concomitant with significant oxidant-antioxidant disturbance and decreased a- and b-wave amplitude in the ERG. These alterations were ameliorated with prior PMG treatment. In conclusion, PMG treatment, as an antioxidant, attenuated retinal structural and functional I/R injury through activation of Nrf2 which could be a base for future therapy designs.
ISSN:0191-3123
1521-0758
DOI:10.1080/01913123.2017.1346737