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We investigated the effects of an ethanol extract of C. denticulatum (EECD) in a mouse model of glaucoma established by optic nerve crush (ONC), and found that EECD significantly protected against retinal ganglion cell (RGC) death caused by ONC. Furthermore, EECD effectively protected against N-methyl-d-aspartate-induced damage to the rat retinas. In vitro, EECD attenuated transformed retinal ganglion cell (RGC-5) death and significantly blunted the up-regulation of apoptotic proteins and mRNA level induced by 1-buthionine-(S,R)-sulfoximine combined with glutamate, reduced reactive oxygen species production by radical species, and inhibited lipid peroxidation. The major EECD components were found to be chicoric acid and 3,5-dicaffeoylquinic acid (3,5-DCQA) that have shown beneficial effects on retinal degeneration both in vitro and in vivo studies. Thus, EECD could be used as a natural neuroprotective agent for glaucoma, and chicoric acid and 3,5-DCQA as mark compounds for the development of functional food.

Improvement of liver function is one of the most popular commercial health claims of functional foods in Asian countries, including Korea. After examining the potential of several traditional Korean wild vegetables for enhancing liver function, we found that Youngia denticulata Kitam. has strong hepatoprotective effects against oxidative stress induced by tert-butylhydroperoxide (t-BHP). We are the first to report that the extract and ethyl acetate fractions of Y. denticulata have radical scavenging activities and inhibit oxidative stress-induced cell death and DNA damage in HepG2 cells. The extract and ethyl acetate fractions significantly decreased cellular reactive oxygen species production and apoptosis induced by t-BHP in HepG2 cells. In addition, they prevented the depletion of cellular glutathione, which is an important defense molecule against oxidizing xenobiotics. Chlorogenic acid and 3,5-dicaffeoylquinic acid were found to be major active components responsible for the activity of Y. denticulata and could serve as marker compounds for standardization. These data suggest that Y. denticulata could be promoted as a potential antioxidative functional food candidate, particularly for hepatoprotection against oxidative stress.

This study was performed to determine whether the compound isolated from Phyllostachys nigra could attenuate oxidative stress in transformed retinal ganglion cells (RGC-5 cells) death. RGC-5 cells in culture were given two different insults such as l-buthionine-(S,R)-sulfoximine (BSO) plus glutamate for 24h or hydrogen peroxide for 24h, after which cell survival were measured. Among the four systematic fractions tested, ethyl acetate fraction showed a significantly higher inhibition which was in a concentration dependent manner. Eight compounds were isolated from ethyl acetate fraction of P. nigra using preparative RP-HPLC and Sephadex LH-20 column chromatography. Their chemical structures were elucidated by chemical and spectral analysis as isoorientin (1), orientin (2), vitexin (3), cis-coumaric acid (4), p-coumaric acid (5), luteolin 6-C-(6''-O-trans-caffeoylglucoside) (6), vittariflavone (7) and tricin (8). The luteolin 6-C-(6''-O-trans-caffeoylglucoside) (compound 6) significantly attenuated the negative effects of BSO plus glutamate or hydrogen peroxide to RGC-5 cells. Treatment of the RGC-5 cells with compound 6 reduced the reactive oxygen species (ROS) as quantified using 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA). This compound also replenished the reduced glutathione level. In conclusion, these results implicate that compound 6 isolated from P. nigra could be used as a leading compounds for retinal disease via anti-oxidative effects., (Copyright 2010 Elsevier Ltd. All rights reserved.)

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. [ABSTRACT FROM AUTHOR]

Abstract: Retinal ganglion cells (RGCs) death caused by oxidative stress is a common risk factor for glaucoma. In the present study, 8-hydroxycalamenene was isolated from the hexane fraction of Reynoutria elliptica. We showed that 8-hydroxycalamenene attenuated the cell death of transformed RGC-5 cells. This compound also produced a dose-dependent decrease in the expression of apoptotic proteins (cleaved PARP and caspase-3) induced by l-buthionine-(S,R)-sulfoximine (BSO) plus glutamate and stimulated glutathione and glutathione S-transferase activity. Moreover, the addition of 8-hydroxycalamenene to cell cultures restored the reduced mitochondrial membrane potential resulting from glutamate/BSO treatment. The presence of N-methyl-d-aspartate in the retina of rats affected the thickness of the inner plexiform layer (IPL) and increased the number of TUNEL-positive RGCs. However, 8-hydroxycalamenene protected against thinning of the IPL and reduced TUNEL-positive cells in the ganglion cell layer. Thus, 8-hydroxycalamenene isolated from R. elliptica exerts neuroprotective effects both in vitro and in vivo. [Copyright &y& Elsevier]

Humulus japonicus is an annual plant belonging to the Cannabacea family, and it has been traditionally used to treat pulmonary tuberculosis, dysentery, chronic colitis, and hypertension. We investigated the active components against Parkinson's disease from H. japonicus fraction (HJF) using high performance liquid chromatography (HPLC) coupled with quadruple-time-of-flight mass spectroscopy (qTOF-MS) and NMR. Fourteen compounds were isolated from HJF, including one new compound, using HPLC-qTOF-MS and NMR. The major compounds of HJF were luteolin-7-O-glucoside and apigenin-7-O-glucoside, and there was approximately 12.57- and 9.68-folds increase in the contents of these flavonoids compared to those of the 70% EtOH extract. Apigenin and luteolin exhibited the strongest inhibitory effects on monoamine oxidase (MAO) B enzyme activity. In animal studies, limb-use behavior was significantly reduced by unilateral 6-OHDA lesion and ipsilateral rotations. These results indicated that oral administration of 300 mg/kg HJF resulted in the improvement of motor asymmetry and motor impairment in unilateral 6-OHDA-lesioned mice. HJF, including active components leads to an improvement of motor behavior in a Parkinson's disease mouse model. [ABSTRACT FROM AUTHOR]