This study explored whether chlorogenic acid (CGA) and coffee have protective effects against retinal degeneration. Under hypoxic conditions, the viability of transformed retinal ganglion (RGC-5) cells was significantly reduced by treatment with the nitric oxide (NO) donor S-nitroso-N-acetylpenicillamine (SNAP). However, pretreatment with CGA attenuated cell death in a concentration-dependent manner. In addition, CGA prevented the up-regulation of apoptotic proteins such as Bad and cleaved caspase-3. Similar beneficial effects of both CGA and coffee extracts were observed in mice that had undergone an optic nerve crush (ONC) procedure. CGA and coffee extract reduced cell death by preventing the down-regulation of Thy-1. Our in vitro and in vivo studies demonstrated that coffee and its major component, CGA, significantly reduce apoptosis of retinal cells induced by hypoxia and NO, and that coffee consumption may help in preventing retinal degeneration.

Baicalin is a flavonoid derived from the dried root of Scutellaria baicalensis. In this study, oxygen-induced retinopathy was used to characterize the anti-angiogenic properties of baicalin in mice. Pups were exposed to a hyperbaric oxygen environment to induce retinal angiogenesis and were subjected to intraperitoneal injection of baicalin. Avascular area, neovascular tufts, and neovascular lumens were quantified from digital images. Compared to the vehicle, baicalin clearly reduced the central avascular zone and the number of neovascular tufts and lumens. High-dose baicalin (10 mg/kg) significantly reduced the expression of matrix metalloproteinase-2 (MMP-2), MMP-9, angiotensin II, and vascular endothelial growth factor (VEGF). These results show that baicalin is a powerful antiangiogenic compound that attenuates new vessel formation in the retina after systemic administration, and is a candidate substance for therapeutic inhibition of retinal angiogenesis. [BMB Reports 2015; 48(5): 271-276]

The purpose of this study was to evaluate the effect of ethanol extract of Diospyros kaki (EEDK) leaves on corneal neovascularization (CoNV) in rats. One week after the alkali burns in the corneas, the CoNV area coverage in the CoNV-positive control group, 100 mg/kg EEDK group, and 200 mg/kg EEDK group was 43.3% -5.5%, 337.7% -2.5%, and 27.2% -4.3%, respectively. The areas of CoNV in the EEDK-treated groups were significantly different from those of the CoNV group. EEDK significantly attenuated the upregulation of vascular endothelial growth factor, fibroblast growth factor, interleukin-6, and matrix metalloproteinase-2 (MMP-2) protein levels. Orally administrated D. kaki inhibited CoNV development in rats.KEY WORDS: alkali burn angiogenic factors corneal neovascularization Diospyros kaki eye diseases C orneal neovascularization (CoNV) is a visionthreatening condition that is usually caused by inflammatory, infectious, or traumatic events at the corneal surface.

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Baicalin suppressed laser-induced CNV formation in rats. These results suggest that baicalin should be considered as a candidate drug for treating exudative age-related macular degeneration.

In the present study, extracts from Rhus verniciflua were demonstrated to significantly attenuate the negative effects of hydrogen peroxide (H 2 O 2 ) on transformed retinal ganglion cell line (RGC-5 cells), indicating that they may be protective against oxidative stress-induced retinal degeneration. The inclusion of R. verniciflua in the culture was found to both reduce the levels of reactive oxygen species (ROS) present and lessen the up-regulation of apoptotic proteins such as cleaved poly(ADP-ribose) polymerase, cleaved caspase-3, and cleaved caspase-9. Active compounds were also successfully isolated from R. verniciflua using high-speed counter-current chromatography (HSCCC) with a two-phase solvent system composed of n-hexane-ethyl acetate-methanol-water (3.5 : 5 : 3.5 : 5, v/v). Using this method, we successfully separated 252.1 mg of fustin at a purity of over 93.09%, 51.2 mg of fisetin at a purity of over 95.45%, 39.7 mg of sulfuretin at a purity of over 95.17%, and 10.7 mg of butein at a purity of over 95.01% from 1.5 g of R. verniciflua extract. The chemical structures of these compounds were elucidated by chemical and spectral analyses. There isolated compounds also significantly attenuated the negative effects of H 2 O 2 on RGC-5 cells. Results therefore suggest that, due to its anti-oxidative and anti-apoptotic effects, R. verniciflua could be used as a lead substance for the treatment of retinal diseases such as glaucoma.

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The luteolin 6‐C‐(6″‐O‐trans‐caffeoylglucoside) (PN6) isolated from Phyllostachys nigra is effective against both the negative influence of N‐methyl‐D‐aspartate (NMDA) to the rat retina and the oxidative stress induced transformed retinal ganglion cells (RGC‐5) death. The PN6 concentration‐dependently inhibited sodium nitroprusside‐induced lipid peroxidation. Treatment of the RGC‐5 with PN6 decreased the apoptotic proteins of poly (adenosine diphosphate‐ribose) polymerase (PARP) and cleaved caspase‐3, and increased the antioxidant proteins of superoxide dismutase (SOD)‐2, catalase and glutathione peroxidase (GPx‐1) expressions by Western blot analysis. The PN6 reduced the thickness of the inner plexiform layer using hematoxylin and eosin staining and decreased the number of terminal deoxynucleotidyl transferase 2′‐deoxyuridine 5′‐triphosphate nick‐end labeling (TUNEL)‐positive cells using TUNEL kit assay. Moreover, PN6 attenuated upregulation of apoptotic proteins (PARP and cleaved caspase‐3) and downregulation of antioxidant proteins (SOD‐2, catalase and GPx‐1) caused by NMDA in the rat retina. Practical Applications The aim of this study was to determine whether the luteolin 6‐C‐(6″‐O‐trans‐caffeoylglucoside) (PN6) previously isolated from Phyllostachys nigra is effective at blunting the negative influence of N‐methyl‐D‐aspartate (NMDA)‐induced excitotoxicity in situ. The treatment of the PN6 was evaluated by lipid peroxidation studies, which showed that PN6 significantly inhibited lipid peroxidation with an half maximal inhibitory concentration (IC50) of 1.05 μM. PN6 decreased the upregulation of poly (adenosine diphosphate‐ribose) polymerase (PARP) and cleaved caspase‐3 and the downregulation of superoxide dismutase (SOD‐2), catalase and glutathione peroxidase (GPx ‐1) in retinal ganglion cells. Intravitreal injection of NMDA to the rat retina reduced the thickness of the inner plexiform layer and increased the number of terminal deoxynucleotidyl transferase 2′‐deoxyuridine 5′‐triphosphate nick‐end labeling‐positive cells, which was partially, but significantly blunted by the presence of PN6. Moreover, PN6 blunted the changes in PARP, cleaved caspase‐3, SOD‐2, catalase and GPx‐1 proteins in the rat retina. Evidence is therefore provided to show that P. nigra can be considered as a candidate neuroprotectant for the treatment of various neurodegenerative diseases.