Green tea extract attenuates MNU-induced photoreceptor cell apoptosis via suppression of heme oxygenase-1

The effects of green tea extract (GTE) on N-methyl-N-nitrosourea (MNU)-induced photoreceptor cell apoptosis were examined, and the possible mechanisms of action of GTE were assessed. Alterations in the retinal morphological architecture were determined by hematoxylin-eosin staining, vimentin immunor...

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Bibliographic Details
Published in:Journal of Toxicologic Pathology 2016, Vol.29(1), pp.61-65
Main Authors: Emoto, Yuko, Yoshizawa, Katsuhiko, Kinoshita, Yuichi, Yuki, Michiko, Yuri, Takashi, Tsubura, Airo
Format: Article
Language:English
Subjects:
Apoptosis
Degeneration
Gene expression
Green tea
green tea extract
Heme
Heme oxygenase (decyclizing)
heme oxygenase-1
Immunoreactivity
Labeling
laser capture microdissection
Marking
Morphology
N-Methyl-N-nitrosourea
Nuclear capture
Oxygenase
photoreceptor cell
Photoreceptors
Rats
Retina
Retinal degeneration
Rodents
Short Communication
Staining
Tea
Vimentin
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Summary:The effects of green tea extract (GTE) on N-methyl-N-nitrosourea (MNU)-induced photoreceptor cell apoptosis were examined, and the possible mechanisms of action of GTE were assessed. Alterations in the retinal morphological architecture were determined by hematoxylin-eosin staining, vimentin immunoreactivity, and photoreceptor cell apoptosis (TUNEL labeling). Expression of oxidant marker, heme oxygenase (HO)-1, mRNA levels in outer nuclear cells was assessed by laser capture microdissection (LCM). Sprague-Dawley rats were given 40 mg/kg MNU at 7 weeks of age in the absence and presence of 250 mg/kg GTE treatment (once daily from 3 days prior to MNU for a maximum 10 days). Although photoreceptor cell degeneration began 24 hr after MNU, the morphological effects of GTE at the time point were not definitive. However, GTE lowered TUNEL labeling and HO-1 mRNA expression. At 7 days after MNU, photoreceptor damage was attenuated by GTE treatment. Therefore, the ability of GTE to reduce MNU-induced photoreceptor cell apoptosis may be due to its antioxidant properties.
ISSN:0914-9198
1881-915X
1347-7404
DOI:10.1293/tox.2015-0052