Abstract
PURPOSE. To investigate the effect of D-allose, a rare sugar, against ischemia reperfusion injury in the rat retina. METHODS. Retinal ischemia was induced by increasing intraocular pressure to 130 mm Hg and maintaining that level for 45 minutes. Morphometric studies were performed to study the effect of D-allose on the histologic changes induced by ischemia in the rat retina. Glutamate release from the rat retina and intravitreal PO2 profiles were monitored during and after ischemia with a microdialysis biosensor and oxygen-sensitive microelectrodes. The release of hydrogen peroxide stained with diaminobenzidine hydrochloride was monitored by an in vitro retinal ischemia model. RESULTS. Seven days after the ischemia, significant reductions in both the number of ganglion cells and the thickness of the inner plexiform layer were observed. Pretreatment with Dallose significantly inhibited the ischemic injury of the inner retina. A large release of glutamate occurred during the ischemia. After the recirculation, glutamate levels were increased again and reached a maximum in approximately 20 minutes. The increases in extracellular glutamate during and after ischemia tend to be suppressed by administration of D-allose. D-Allose attenuated the increase in intravitreal PO2 during reperfusion. After the ischemia, production of hydrogen peroxide was detected within approximately 30 minutes. D-Allose suppressed the production of hydrogen peroxide. CONCLUSIONS. These results suggest that D-allose may protect neurons by decreasing extracellular glutamate and attenuating oxidative stress in ischemic insult.
| Original language | English |
|---|---|
| Pages (from-to) | 1653-1657 |
| Number of pages | 5 |
| Journal | Investigative Ophthalmology and Visual Science |
| Volume | 47 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - Apr 2006 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Ophthalmology
Cite this
Neuroprotective effects of D-allose against retinal ischemia-reperfusion injury. / Hirooka, Kazuyuki; Miyamoto, Osamu; Jinming, Pan; Du, Yinghua; Itano, Toshifumi; Baba, Tetsuya; Tokuda, Masaaki; Shiraga, Fumio.
In: Investigative Ophthalmology and Visual Science, Vol. 47, No. 4, 04.2006, p. 1653-1657.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Neuroprotective effects of D-allose against retinal ischemia-reperfusion injury
AU - Hirooka, Kazuyuki
AU - Miyamoto, Osamu
AU - Jinming, Pan
AU - Du, Yinghua
AU - Itano, Toshifumi
AU - Baba, Tetsuya
AU - Tokuda, Masaaki
AU - Shiraga, Fumio
PY - 2006/4
Y1 - 2006/4
N2 - PURPOSE. To investigate the effect of D-allose, a rare sugar, against ischemia reperfusion injury in the rat retina. METHODS. Retinal ischemia was induced by increasing intraocular pressure to 130 mm Hg and maintaining that level for 45 minutes. Morphometric studies were performed to study the effect of D-allose on the histologic changes induced by ischemia in the rat retina. Glutamate release from the rat retina and intravitreal PO2 profiles were monitored during and after ischemia with a microdialysis biosensor and oxygen-sensitive microelectrodes. The release of hydrogen peroxide stained with diaminobenzidine hydrochloride was monitored by an in vitro retinal ischemia model. RESULTS. Seven days after the ischemia, significant reductions in both the number of ganglion cells and the thickness of the inner plexiform layer were observed. Pretreatment with Dallose significantly inhibited the ischemic injury of the inner retina. A large release of glutamate occurred during the ischemia. After the recirculation, glutamate levels were increased again and reached a maximum in approximately 20 minutes. The increases in extracellular glutamate during and after ischemia tend to be suppressed by administration of D-allose. D-Allose attenuated the increase in intravitreal PO2 during reperfusion. After the ischemia, production of hydrogen peroxide was detected within approximately 30 minutes. D-Allose suppressed the production of hydrogen peroxide. CONCLUSIONS. These results suggest that D-allose may protect neurons by decreasing extracellular glutamate and attenuating oxidative stress in ischemic insult.
AB - PURPOSE. To investigate the effect of D-allose, a rare sugar, against ischemia reperfusion injury in the rat retina. METHODS. Retinal ischemia was induced by increasing intraocular pressure to 130 mm Hg and maintaining that level for 45 minutes. Morphometric studies were performed to study the effect of D-allose on the histologic changes induced by ischemia in the rat retina. Glutamate release from the rat retina and intravitreal PO2 profiles were monitored during and after ischemia with a microdialysis biosensor and oxygen-sensitive microelectrodes. The release of hydrogen peroxide stained with diaminobenzidine hydrochloride was monitored by an in vitro retinal ischemia model. RESULTS. Seven days after the ischemia, significant reductions in both the number of ganglion cells and the thickness of the inner plexiform layer were observed. Pretreatment with Dallose significantly inhibited the ischemic injury of the inner retina. A large release of glutamate occurred during the ischemia. After the recirculation, glutamate levels were increased again and reached a maximum in approximately 20 minutes. The increases in extracellular glutamate during and after ischemia tend to be suppressed by administration of D-allose. D-Allose attenuated the increase in intravitreal PO2 during reperfusion. After the ischemia, production of hydrogen peroxide was detected within approximately 30 minutes. D-Allose suppressed the production of hydrogen peroxide. CONCLUSIONS. These results suggest that D-allose may protect neurons by decreasing extracellular glutamate and attenuating oxidative stress in ischemic insult.
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U2 - 10.1167/iovs.05-1018
DO - 10.1167/iovs.05-1018
M3 - Article
VL - 47
SP - 1653
EP - 1657
JO - Investigative Ophthalmology and Visual Science
JF - Investigative Ophthalmology and Visual Science
SN - 0146-0404
IS - 4
ER -