The ophthalmic artery occlusion and blood resupply by ECA and ICA can be easily monitored by the duration of filament kept inside the vessel lumen. This model induces complete but R428 distributor reversible retinal ischemia injury and leads to a considerable cell loss in inner TWS119 retina by the blockade of ophthalmic artery. It mimics the clinical situation of transient monocular amaurosis fugax and other ocular diseases in which retinal I/R is a complication. Therefore, this artery occlusion model is a good tool for exploring neuroprotective agents against retinal I/R injury. Lycium barbarum is a dried fruit that is used as a food or a medicine according to Chinese tradition. It has been claimed that LBP can exhibit anti-aging, anti-tumor, cytoprotective, neuromodulation, and immune modulation effects. LBP can attenuate breakage of DNA by oxidation in the testicle cells in mice. It has also been shown to protect DNA damage of peripheral blood lymphocytes against oxidative stress. However, researches on the protective effects of LBP against ocular diseases are still ongoing. In the present study, we aim to look at the protective effects of LBP against retinal I/R injury. We focus on four aspects that are closely related to retinal I/R injury: anti-apoptosis, preservation of BRB integrity, prevention of retinal swelling, and anti-oxidation. Retinal I/R induces neuronal death in the inner retina, especially RGC. An extensive loss of cells in the GCL has been seen after retinal I/R injury. A majority of these neurons die by apoptosis during retinal I/R injury. Our data show an increased number of apoptotic nuclei in inner retinal layers, especially in the GCL, of the ischemic retina. The result is highly reproducible and comparable to our previously published data. In previous studies, only a few TUNEL-positive apoptotic cells are found in inner retina with 1 hr ischemia injury although similar animal model is used. The discrepancy is probably due to the shorter ischemia period when compared with that in our study. Retinal function, assessed by the a-wave and b-wave of electroretinography, is deteriorated in the ischemic eye, suggesting that the function of retinal neurons is weakened in retinal I/R injury. Similar to a previous study, we also show that retinal I/R caused detrimental injury to amacrine cells, as indicated by the great reduction in calretinin expression and the dis-organization of IPL stratification. Apart from calretininexpressing amacrine cells, fewer nNOS-expressing amacrine cells were observed in I/R retina. Comparable phenomenon was noted in bipolar cell immunoreactivity in the present study. Apart from neuronal damage, I/R injury also induces impairment in synaptic connections of retinal neurons.