scholarly journals Icarin Levels using HPLC/MS and Antioxidant and neuronal PC12 cell protective effects from Epimedium koreanum on hydrogen peroxide‐induced oxidative damage

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Miran Jang ◽  
Gun‐Hee Kim
RSC Advances ◽  
2017 ◽  
Vol 7 (28) ◽  
pp. 17377-17386 ◽  
Author(s):  
Ting Xia ◽  
Jiahui Yao ◽  
Jin Zhang ◽  
Yu Zheng ◽  
Jia Song ◽  
...  

Shanxi aged vinegar (SAV), a kind of typical fermented food, is one of the famous traditional vinegars in China.


Life Sciences ◽  
2004 ◽  
Vol 75 (10) ◽  
pp. 1263-1276 ◽  
Author(s):  
Juana Benedı́ ◽  
Rocio Arroyo ◽  
Carmen Romero ◽  
Sagrario Martı́n-Aragón ◽  
Angel M Villar

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 1067 ◽  
Author(s):  
Faith A. Kwa ◽  
Nabeela K. Dulull ◽  
Ute Roessner ◽  
Daniel A. Dias ◽  
Thusitha W. Rupasinghe

Background: Age-related macular degeneration (AMD) is a leading cause of blindness in the ageing population. Without effective treatment strategies that can prevent disease progression, there is an urgent need for novel therapeutic interventions to reduce the burden of vision loss and improve patients’ quality of life. Dysfunctional innate immune responses to oxidative stress observed in AMD can be caused by the formation of oxidised lipids, whilst polyunsaturated fatty acids have shown to increase the risk of AMD and disease progression in affected individuals. Previously, our laboratory has shown that the vegetable-derived isothiocyanate, L-sulforaphane (LSF), can protect human adult pigment epithelial cells from oxidative damage by upregulating gene expression of the oxidative stress enzyme Glutathione-S-Transferase µ1. This study aims to validate the protective effects of LSF on human retinal cells under oxidative stress conditions and to reveal the key players in fatty acid and lipid metabolism that may facilitate this protection. Methods: The in vitro oxidative stress model of AMD was based on the exposure of an adult retinal pigment epithelium-19 cell line to 200µM hydrogen peroxide. Percentage cell proliferation following LSF treatment was measured using tetrazolium salt-based assays. Untargeted fatty acid profiling was performed by gas chromatography-mass spectrometry. Untargeted lipid profiling was performed by liquid chromatography-mass spectrometry. Results: Under hydrogen peroxide-induced oxidative stress conditions, LSF treatment induced dose-dependent cell proliferation. The key fatty acids that were increased by LSF treatment of the retinal cells include oleic acid and eicosatrienoic acid. LSF treatment also increased levels of the lipid classes phosphatidylcholine, cholesteryl ester and oxo-phytodienoic acid but decreased levels of phosphatidylethanolamine lipids. Conclusions: We propose that retinal cells at risk of oxidative damage and apoptosis can be pre-conditioned with LSF to regulate levels of selected fatty acids and lipids known to be implicated in the pathogenesis and progression of AMD.


F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 1067
Author(s):  
Faith A. Kwa ◽  
Nabeela K. Dulull ◽  
Ute Roessner ◽  
Daniel A. Dias ◽  
Thusitha W. Rupasinghe

Background: Age-related macular degeneration (AMD) is a leading cause of blindness in the ageing population. Without effective treatment strategies that can prevent disease progression, there is an urgent need for novel therapeutic interventions to reduce the burden of vision loss and improve patients’ quality of life. Dysfunctional innate immune responses to oxidative stress observed in AMD can be caused by the formation of oxidised lipids, whilst polyunsaturated fatty acids have shown to increase the risk of AMD and disease progression in affected individuals. Previously, our laboratory has shown that the vegetable-derived isothiocyanate, L-sulforaphane (LSF), can protect human adult pigment epithelial cells from oxidative damage by upregulating gene expression of the oxidative stress enzyme Glutathione-S-Transferase µ1. This study aims to validate the protective effects of LSF on human retinal cells under oxidative stress conditions and to reveal the key players in fatty acid and lipid metabolism that may facilitate this protection. Methods: The in vitro oxidative stress model of AMD was based on the exposure of an adult retinal pigment epithelium-19 cell line to 200µM hydrogen peroxide. Percentage cell proliferation following LSF treatment was measured using tetrazolium salt-based assays. Untargeted fatty acid profiling was performed by gas chromatography-mass spectrometry. Untargeted lipid profiling was performed by liquid chromatography-mass spectrometry. Results: Under hydrogen peroxide-induced oxidative stress conditions, LSF treatment induced dose-dependent cell proliferation. The key fatty acids that were increased by LSF treatment of the retinal cells include oleic acid and eicosatrienoic acid. LSF treatment also increased levels of the lipid classes phosphatidylcholine, cholesteryl ester and oxo-phytodienoic acid but decreased levels of phosphatidylethanolamine lipids. Conclusions: We propose that retinal cells at risk of oxidative damage and apoptosis can be pre-conditioned with LSF to regulate levels of selected fatty acids and lipids known to be implicated in the pathogenesis and progression of AMD.


2017 ◽  
Vol 36 (9) ◽  
pp. 967-980 ◽  
Author(s):  
SB Mada ◽  
S Reddi ◽  
N Kumar ◽  
S Kapila ◽  
R Kapila

Oxidative stress inhibits osteoblast differentiation and function that lead to the development of osteoporosis. Casein-derived peptide VLPVPQK (PEP), a potent antioxidant, was isolated from β-casein of buffalo milk. We used an in vitro oxidative stress model induced by hydrogen peroxide (H2O2) in rat osteoblastic cells to investigate the protective effects of PEP against H2O2-induced dysfunction and oxidative damage. Cells were pretreated with PEP (50–200 ng/mL) for 2, 7 or 21 days followed by 0.3 mM H2O2 treatment for 24 h and then markers of osteogenic development, oxidative damage and apoptosis were examined. PEP significantly increased the viability and differentiation markers of osteoblast cells such as alkaline phosphatase and calcium mineralization. Moreover, PEP suppressed the production of reactive oxygen species (ROS), lipid peroxidation and ameliorated H2O2-induced reduction in glutathione, superoxide dismutase and catalase activities. In addition, PEP partially inhibited caspase-9 and-3 activities and reduced propidium iodide–positive cells. Altogether, our results demonstrated that PEP could protect rat osteoblast against H2O2-induced dysfunction and oxidative damage by reduction of ROS production, lipid peroxidation and increased antioxidant enzyme activities. Thus, our data suggest that PEP might be a valuable protective agent against oxidative stress–related diseases such as osteoporosis.


2011 ◽  
Vol 89 (6) ◽  
pp. 445-453 ◽  
Author(s):  
Tao Chen ◽  
Zai-pei Guo ◽  
Xiao-yan Jiao ◽  
Yu-hong Zhang ◽  
Jing-yi Li ◽  
...  

Peoniflorin (PF), extracted from the root of Paeonia lactiflora Pall., has been reported to have anti-inflammation and antioxidant effects in several animal models. Herein, we investigated the protective effects of PF against hydrogen peroxide (H2O2)-induced oxidative damage in human umbilical vein endothelial cells (HUVECs). HUVECs were treated by H2O2 (240 µmol/L) with or without PF. PF significantly increased the percent cell viability of HUVECs injured by H2O2 using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. By flow cytometric analysis, PF markedly attenuated H2O2-induced apoptosis and intracellular reactive oxygen species production. In addition, PF also displayed a dose-dependent reduction of lactate dehydrogenase leakage, malondialdehyde formation, and caspase-3 proteolytic activities in H2O2-treated cells, which was accompanied with a restoration of the activities of endogenous antioxidants, including total superoxide dismutase and glutathione peroxidase. Finally, Western blot data revealed that H2O2 upregulated phosphorylation of extracellular signal-regulated kinase 1/2 in HUVECs, which was almost completely reversed by PF. Taken together, our data provide the first evidence that PF has a protective ability against oxidative damage in HUVECs. PF may be a candidate medicine for the treatment of vascular diseases associated with oxidative stress.


F1000Research ◽  
2020 ◽  
Vol 8 ◽  
pp. 1067
Author(s):  
Faith A. Kwa ◽  
Nabeela K. Dulull ◽  
Ute Roessner ◽  
Daniel A. Dias ◽  
Thusitha W. Rupasinghe

Background: Age-related macular degeneration (AMD) is a leading cause of blindness in the ageing population. Without effective treatment strategies that can prevent disease progression, there is an urgent need for novel therapeutic interventions to reduce the burden of vision loss and improve patients’ quality of life. Dysfunctional innate immune responses to oxidative stress observed in AMD can be caused by the formation of oxidised lipids, whilst polyunsaturated fatty acids have shown to increase the risk of AMD and disease progression in affected individuals. Previously, our laboratory has shown that the vegetable-derived isothiocyanate, L-sulforaphane (LSF), can protect human adult pigment epithelial cells from oxidative damage by upregulating gene expression of the oxidative stress enzyme Glutathione-S-Transferase µ1. This study aims to validate the protective effects of LSF on human retinal cells under oxidative stress conditions and to reveal the key players in fatty acid and lipid metabolism that may facilitate this protection. Methods: The in vitro oxidative stress model of AMD was based on the exposure of an adult retinal pigment epithelium-19 cell line to 200µM hydrogen peroxide. Percentage cell proliferation following LSF treatment was measured using tetrazolium salt-based assays. Untargeted fatty acid profiling was performed by gas chromatography-mass spectrometry. Untargeted lipid profiling was performed by liquid chromatography-mass spectrometry. Results: Under hydrogen peroxide-induced oxidative stress conditions, LSF treatment induced dose-dependent cell proliferation. The key fatty acids that were increased by LSF treatment of the retinal cells include oleic acid and eicosatrienoic acid. LSF treatment also increased levels of the lipid classes phosphatidylcholine, cholesteryl ester and oxo-phytodienoic acid but decreased levels of phosphatidylethanolamine lipids. Conclusions: We propose that retinal cells at risk of oxidative damage and apoptosis can be pre-conditioned with LSF to regulate levels of selected fatty acids and lipids known to be implicated in the pathogenesis and progression of AMD.


F1000Research ◽  
2020 ◽  
Vol 8 ◽  
pp. 1067
Author(s):  
Faith A. Kwa ◽  
Nabeela K. Dulull ◽  
Ute Roessner ◽  
Daniel A. Dias ◽  
Thusitha W. Rupasinghe

Background: Age-related macular degeneration (AMD) is a leading cause of blindness in the ageing population. Without effective treatment strategies that can prevent disease progression, there is an urgent need for novel therapeutic interventions to reduce the burden of vision loss and improve patients’ quality of life. Dysfunctional innate immune responses to oxidative stress observed in AMD can be caused by the formation of oxidised lipids, whilst polyunsaturated fatty acids have shown to increase the risk of AMD and disease progression in affected individuals. Previously, our laboratory has shown that the vegetable-derived isothiocyanate, L-sulforaphane (LSF), can protect human adult pigment epithelial cells from oxidative damage by upregulating gene expression of the oxidative stress enzyme Glutathione-S-Transferase µ1. This study aims to validate the protective effects of LSF on human retinal cells under oxidative stress conditions and to reveal the key players in fatty acid and lipid metabolism that may facilitate this protection. Methods: The in vitro oxidative stress model of AMD was based on the exposure of an adult retinal pigment epithelium-19 cell line to 200µM hydrogen peroxide. Percentage cell proliferation following LSF treatment was measured using tetrazolium salt-based assays. Untargeted fatty acid profiling was performed by gas chromatography-mass spectrometry. Untargeted lipid profiling was performed by liquid chromatography-mass spectrometry. Results: Under hydrogen peroxide-induced oxidative stress conditions, LSF treatment induced dose-dependent cell proliferation. The key fatty acids that were increased by LSF treatment of the retinal cells include oleic acid and eicosatrienoic acid. LSF treatment also increased levels of the lipid classes phosphatidylcholine, cholesteryl ester and oxo-phytodienoic acid but decreased levels of phosphatidylethanolamine lipids. Conclusions: We propose that retinal cells at risk of oxidative damage and apoptosis can be pre-conditioned with LSF to regulate levels of selected fatty acids and lipids known to be implicated in the pathogenesis and progression of AMD.


2005 ◽  
Vol 383 (3) ◽  
pp. 256-259 ◽  
Author(s):  
Zhi-Hua Chen ◽  
Yasukazu Yoshida ◽  
Yoshiro Saito ◽  
Etsuo Niki

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