Compound Isolated from the Leaves of Phyllostachys nigra Protects NMDA-Induced Retinal Degeneration

Authors


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Abstract

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.

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