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Caffeic acid phenethyl ester protects 661W cells from H2O2-mediated cell death and enhances electroretinography response in dim-reared albino rats.

Chen H, Tran JT, Anderson RE, Mandal MN - Mol. Vis. (2012)

Bottom Line: Caffeic acid phenethyl ester (CAPE), an active component of honeybee propolis, has a wide range of beneficial properties.Pretreatment of 661W cells with CAPE reduced H(2)O(2)-mediated cell death in a dose-dependent manner and induced expression of heme oxygenase-1 (Ho1).CAPE can activate the antioxidative gene expression pathway in retinal cells in vitro and in vivo.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.

ABSTRACT

Purpose: Caffeic acid phenethyl ester (CAPE), an active component of honeybee propolis, has a wide range of beneficial properties. The purpose of this study was to test the protective role of CAPE in 661W cells (in vitro) against H(2)O(2)-mediated cell death and in albino rats (in vivo) against various light conditions.

Methods: The 661W cells were pretreated with CAPE and then stressed with H(2)O(2). Cell death was measured with lactate dehydrogenase (LDH) release assay, and mRNA and proteins were analyzed. Sprague Dawley rats were raised on either a control or CAPE (0.02%) diet and exposed to various light conditions for short or long periods. Retinal histology, mRNA, protein, lipid composition, and retinal function by electroretinography (ERG) were measured at the end of feeding.

Results: Pretreatment of 661W cells with CAPE reduced H(2)O(2)-mediated cell death in a dose-dependent manner and induced expression of heme oxygenase-1 (Ho1). Albino rats fed with CAPE had greater expression of Ho1 and intercellular adhesion molecule 1 (Icam1), less expression of FOS-like antigen (Fosl) and lipoxygenase 12 (Lox12) genes in the retina, less translocation of nuclear factor kappaB protein to the nucleus, and a lower molar ratio of n-3 polyunsaturated fatty acids. Further, the ERGs of the retinas of CAPE-fed rats were significantly higher than those of the control-fed rats when raised in dim light.

Conclusions: CAPE can activate the antioxidative gene expression pathway in retinal cells in vitro and in vivo. Feeding CAPE to albino rats can enhance ERG responses and change the lipid profile in the rats' retinas.

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Related in: MedlinePlus

Caffeic acid phenethyl ester (CAPE) protects 661W cells from oxidant-induced cell death. 661W cells were pretreated in situ with 1 to 20 μM CAPE for 3 h. After thorough washing, cells were exposed to 1 mM H2O2 for 6 h. Cell death was then measured by analyzing the release of lactate dehydrogenase (LDH; n=4 plate × 4 replication assay). (*: p<0.01; **: p<0.001; by one way ANOVA)
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f1: Caffeic acid phenethyl ester (CAPE) protects 661W cells from oxidant-induced cell death. 661W cells were pretreated in situ with 1 to 20 μM CAPE for 3 h. After thorough washing, cells were exposed to 1 mM H2O2 for 6 h. Cell death was then measured by analyzing the release of lactate dehydrogenase (LDH; n=4 plate × 4 replication assay). (*: p<0.01; **: p<0.001; by one way ANOVA)

Mentions: The 661W cells were pretreated with varied doses of CAPE (from 1 to 20 µM) for 3 h, washed the cells, waited 3 h, and then challenged the cells with 1 mM H2O2 for 6 h. This oxidant challenge caused 27% cell death. Pretreatment with CAPE reduced the cell death in a dose-dependent manner up to 5 μM (Figure 1). The cells were then harvested and extracted the mRNA and proteins. An analysis was conducted for the expression of the genes involved in oxidative stress and the proteins involved in apoptotic and protective signaling.


Caffeic acid phenethyl ester protects 661W cells from H2O2-mediated cell death and enhances electroretinography response in dim-reared albino rats.

Chen H, Tran JT, Anderson RE, Mandal MN - Mol. Vis. (2012)

Caffeic acid phenethyl ester (CAPE) protects 661W cells from oxidant-induced cell death. 661W cells were pretreated in situ with 1 to 20 μM CAPE for 3 h. After thorough washing, cells were exposed to 1 mM H2O2 for 6 h. Cell death was then measured by analyzing the release of lactate dehydrogenase (LDH; n=4 plate × 4 replication assay). (*: p<0.01; **: p<0.001; by one way ANOVA)
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3369890&req=5

f1: Caffeic acid phenethyl ester (CAPE) protects 661W cells from oxidant-induced cell death. 661W cells were pretreated in situ with 1 to 20 μM CAPE for 3 h. After thorough washing, cells were exposed to 1 mM H2O2 for 6 h. Cell death was then measured by analyzing the release of lactate dehydrogenase (LDH; n=4 plate × 4 replication assay). (*: p<0.01; **: p<0.001; by one way ANOVA)
Mentions: The 661W cells were pretreated with varied doses of CAPE (from 1 to 20 µM) for 3 h, washed the cells, waited 3 h, and then challenged the cells with 1 mM H2O2 for 6 h. This oxidant challenge caused 27% cell death. Pretreatment with CAPE reduced the cell death in a dose-dependent manner up to 5 μM (Figure 1). The cells were then harvested and extracted the mRNA and proteins. An analysis was conducted for the expression of the genes involved in oxidative stress and the proteins involved in apoptotic and protective signaling.

Bottom Line: Caffeic acid phenethyl ester (CAPE), an active component of honeybee propolis, has a wide range of beneficial properties.Pretreatment of 661W cells with CAPE reduced H(2)O(2)-mediated cell death in a dose-dependent manner and induced expression of heme oxygenase-1 (Ho1).CAPE can activate the antioxidative gene expression pathway in retinal cells in vitro and in vivo.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.

ABSTRACT

Purpose: Caffeic acid phenethyl ester (CAPE), an active component of honeybee propolis, has a wide range of beneficial properties. The purpose of this study was to test the protective role of CAPE in 661W cells (in vitro) against H(2)O(2)-mediated cell death and in albino rats (in vivo) against various light conditions.

Methods: The 661W cells were pretreated with CAPE and then stressed with H(2)O(2). Cell death was measured with lactate dehydrogenase (LDH) release assay, and mRNA and proteins were analyzed. Sprague Dawley rats were raised on either a control or CAPE (0.02%) diet and exposed to various light conditions for short or long periods. Retinal histology, mRNA, protein, lipid composition, and retinal function by electroretinography (ERG) were measured at the end of feeding.

Results: Pretreatment of 661W cells with CAPE reduced H(2)O(2)-mediated cell death in a dose-dependent manner and induced expression of heme oxygenase-1 (Ho1). Albino rats fed with CAPE had greater expression of Ho1 and intercellular adhesion molecule 1 (Icam1), less expression of FOS-like antigen (Fosl) and lipoxygenase 12 (Lox12) genes in the retina, less translocation of nuclear factor kappaB protein to the nucleus, and a lower molar ratio of n-3 polyunsaturated fatty acids. Further, the ERGs of the retinas of CAPE-fed rats were significantly higher than those of the control-fed rats when raised in dim light.

Conclusions: CAPE can activate the antioxidative gene expression pathway in retinal cells in vitro and in vivo. Feeding CAPE to albino rats can enhance ERG responses and change the lipid profile in the rats' retinas.

Show MeSH
Related in: MedlinePlus