Yinghua Du

Publications (2)5.11 Total impact

• Article: Both amacrine and bipolar cells release glutamate in the rat retina after ischemia/reperfusion insult in vitro.

  Yinghua Du, Kazuyuki Hirooka, Osamu Miyamoto, Toshifumi Itano, Masaaki Tokuda, Fumio Shiraga
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  ABSTRACT: To investigate which cells in the inner nuclear layer release glutamate after exposure through the use of a model mimicking rat retina ischemia/reperfusion induced by glucose/oxygen deprivation in vitro. An in vitro retinal ischemia model was used to monitor the release of glutamate by staining with diaminobenzidine hydrochloride. Immunocytochemistry was used to identify the cells releasing glutamate during ischemic/reperfusion injury. On immunocytochemistry, double-labeling of some amacrine and bipolar cells was observed, with somata being stained blue by GABA and two portions of the processes labeled brown due to glutamate reactivity. Some somata of amacrine cells were double-labeled with calbindin, while horizontal cells were single-labeled with calbindin. During ischemia/reperfusion injury in vitro, both amacrine and bipolar cells release glutamate. These results may be related to the patterns of apoptotic cell death seen in the inner retina.
  Current eye research 10/2008; 33(9):782-8. · 1.51 Impact Factor
• Article: Neuroprotective effects of D-allose against retinal ischemia-reperfusion injury.

  Kazuyuki Hirooka, Osamu Miyamoto, Pan Jinming, Yinghua Du, Toshifumi Itano, Tetsuya Baba, Masaaki Tokuda, Fumio Shiraga
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  ABSTRACT: To investigate the effect of D-allose, a rare sugar, against ischemia reperfusion injury in the rat retina. 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 P(O2) 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. 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 D-allose 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 P(O2) during reperfusion. After the ischemia, production of hydrogen peroxide was detected within approximately 30 minutes. D-allose suppressed the production of hydrogen peroxide. These results suggest that D-allose may protect neurons by decreasing extracellular glutamate and attenuating oxidative stress in ischemic insult.
  Investigative Ophthalmology &amp Visual Science 05/2006; 47(4):1653-7. · 3.60 Impact Factor