-
[show abstract]
[hide abstract]
ABSTRACT: Chronic exposure of the skin to ultraviolet B (UVB) radiation induces oxidative stress, which plays a crucial role in the induction of skin cancer. The brown alga Undaria crenata is a potential source of antioxidant and anti-apoptotic compounds due to its capacity to produce protective compounds against environmental factors, including UV radiation. The aim of this study was to investigate the photoprotective properties of an U.crenata ethanol extract (UCE) against UVB-induced cell damage in human HaCaT keratinocytes. UCE exhibited absorbing effect of UVB (280-320 nm) and scavenging activity against the 1,1-diphenyl-2-picrylhydrazyl radical and intracellular reactive oxygen species induced by hydrogen peroxide and UVB rays. Furthermore, electron spin resonance spectrometry revealed the significant scavenging effect of UCE against superoxide anion and hydroxyl radical. UCE reduced UVB-induced apoptosis, as shown by a decrease in apoptotic bodies and nuclear and DNA fragmentation, resulting in the recovery of cell viability. UCE also decreased the degree of UVB-induced oxidative stress to lipids, proteins, and DNA as shown by a decrease in 8-isoprostane level, protein carbonylation and DNA tails. These results suggest that UCE protects human keratinocytes against UVB-induced oxidative stress.
Journal of Bioscience and Bioengineering 03/2013; · 1.79 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Ultraviolet B generates reactive oxygen species by interacting with water in irradiated skin tissues and cells in turn causes lipid peroxidation, protein modification and further DNA damage.
This study examined the cytoprotective effects of phloroglucinol (1,3,5-trihydroxybenzene) on ultraviolet B-irradiated cultured human keratinocytes.
The human keratinocyte cell line HaCaT cells were treated with 10 μM of phloroglucinol. After 1 h, the cells were irradiated with ultraviolet B light at 30 mJ/cm(2) and incubated at 37°C.
Phloroglucinol scavenged both the superoxide anion and hydroxyl radical in a cell-free system and ultraviolet B-induced intracellular reactive oxygen species. Phloroglucinol reduced ultraviolet B-generated lipid peroxidation, protein modification and DNA strand breaks. The enzymatic effects of phloroglucinol restored cellular glutathione levels, superoxide dismutase and catalase activities, which were impaired by ultraviolet B radiation.
Phloroglucinol provides the protective effects in human keratinocyte cell line exposed to ultraviolet B radiation, suggesting that phloroglucinol can be used as a photoprotective agent.
Photodermatology Photoimmunology and Photomedicine 12/2012; 28(6):322-31. · 1.30 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The aim of this study was to investigate the protective effects of the ethanol extract of the red algae Chondracanthus tenellus (Harvey) Hommersand (CTE) on cultured human keratinocyte cell line. The cellular protection conferred by CTE was evidenced by the ability of the extract to absorb ultraviolet B (UVB; 280-320 nm) and to scavenge the radical 1,1-diphenyl-2-picrylhydrazyl, as well as intracellular reactive oxygen species (ROS), induced by either hydrogen peroxide (H(2)O(2)) or UVB radiation. In addition, both superoxide anion generated by the xanthine/xanthine oxidase system and hydroxyl radical generated by the Fenton reaction (FeSO(4) + H(2)O(2)) were scavenged by CTE, as confirmed using electron spin resonance spectrometry. In the human keratinocyte cell line, CTE decreased the degree of injury resulting from UVB-induced oxidative stress to lipids, proteins, and DNA. CTE-treated cells also showed a reduction in UVB-induced apoptosis, as exemplified by fewer apoptotic bodies and less DNA fragmentation. Taken together, these results suggest that CTE confers protection on the human keratinocyte cell line against UVB-induced oxidative stress by absorbing UVB ray and scavenging ROS, thereby reducing injury to cellular constituents.
In Vitro Cellular & Developmental Biology - Animal 10/2012; · 1.31 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Exposure of the skin to ultraviolet B (UVB) radiation leads to epidermal damage and the generation of reactive oxygen species (ROS) in skin cells, including keratinocytes. Therefore, the photo-protective effect of 3-bromo-4, 5-dihydroxybenzaldehyde (BDB) against UVB was assessed in human HaCaT keratinocytes exposed to UVB radiation in vitro. BDB restored cell viability, which decreased upon exposure to UVB radiation. BDB exhibited scavenging activity against 1, 1-diphenyl-2-picrylhydrazyl radicals, intracellular ROS induced by hydrogen peroxide (H(2)O(2)) or UVB radiation, the superoxide anion generated by the xanthine/xanthine oxidase system, and the hydroxyl radical generated by the Fenton reaction (FeSO(4)+H(2)O(2)). Moreover, BDB absorbed UVB and decreased injury resulting from UVB-induced oxidative stress to lipids, proteins and DNA. Finally, BDB reduced UVB-induced apoptosis, as exemplified by fewer apoptotic bodies and a reduction in DNA fragmentation. Taken together, these results suggest that BDB protects human keratinocytes against UVB-induced oxidative stress by scavenging ROS and absorbing UVB rays, thereby reducing injury to cellular components.
Ecotoxicology and Environmental Safety 07/2012; 83:71-8. · 2.29 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: KIOM-4 is a plant extract obtained from Magnolia officinalis, Pueraria lobata, Glycyrrhiza uralensis, and Euphorbia pekinensis. Previously, we reported that KIOM-4 protects pancreatic β-cells against streptozotocin (STZ) induced oxidative stress. To
elucidate the cytoprotective mechanism of KIOM-4 on oxidative stress, we focused on the induction of heme oxygenase-1 (HO-1),
which plays a role in cytoprotection against oxidative injury as well as providing an important function in the maintenance
of homeostasis, in rat pancreatic β-cells (RINm5F). In this study, we showed that KIOM-4 up-regulated HO-1 expression at the
mRNA and protein levels, thus resulting in increased HO-1 activity. HO-1 induction is regulated at the transcriptional level
and is mediated by a specific enhancer, the antioxidant response element (ARE), which is found in the promoter of HO-1 gene.
The transcription factor, NF-E2 related factor 2 (Nrf2), interacts with the ARE to activate HO-1 gene transcription and results
in the modulation of HO-1 expression. KIOM-4 increased the nuclear translocation, ARE binding, and transcriptional activity
of Nrf2. In addition, the extracellular regulated kinase (ERK) positively contributed to ARE-driven HO-1 expression. Furthermore,
KIOM-4 elicited the activation of ERK and U0126 (inhibitor of ERK) attenuated the KIOM-4 induced activation of Nrf2, which
subsequently decreased HO-1 protein levels. These findings suggest that the induction of HO-1 by KIOM-4 is dependent on the
ERK pathway. Taken together, KIOM-4 enhances the cellular antioxidant defense system through the induction of HO-1 via the ERK-Nrf2-ARE signaling pathway, thereby protecting cells from streptozotocin-induced cell damage.
Biotechnology and Bioprocess Engineering 04/2012; 14(3):295-301. · 1.28 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: 8-Hydroxydeoxyguanosine (oh8dG) treatment induced senescence-like changes in KG-1 cells, a human acute myelocytic leukemia cell line. The oh8dG-treated cells stained positive for senescence associated β-galactosidase (SA-β-galactosidase) and had enlarged cell shape,
both of which are senescence indexes. The oh8dG-treated cells were also cell growth inhibited and arrested at G1 in the cell cycle. The accumulation of cdk (cyclin dependent kinase) inhibitors, such as p16, p21, and p27, also implies
that cellular senescence was induced in oh8dG-treated cells. However, these changes were not accompanied by cell differentiation or telomerase activity. Taken together,
we conclude that oh8dG treatment of KG-1 cells induces cellular senescence.
Biotechnology and Bioprocess Engineering 04/2012; 12(2):114-120. · 1.28 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Excessive amounts of reactive oxygen species (ROS) induced by ultraviolet (UV) radiation cause skin aging via basement membrane/extracellular matrix degradation resulting from the action of matrix metalloproteinases (MMPs). Recently, phloroglucinol (1,3,5-trihydroxybenzene) was demonstrated to attenuate the cell damage induced by oxidative stress by quenching ROS and stimulating antioxidant systems. In the current study, the effect of phloroglucinol on UVB-induced photoaging was investigated in human HaCaT keratinocytes. Phloroglucinol significantly inhibited the UVB-induced (1) upregulation of MMP-1 mRNA, protein and activity; (2) augmentation of intracellular Ca(2+) levels; (3) phosphorylation of mitogen-activated protein kinases (MAPKs); (4) expression of c-Fos and phospho c-Jun; and (5) enhancement of activator protein-1 (AP-1) binding to the MMP-1 promoter. In addition, the knockdown of MAPKs significantly inhibited UVB-induced MMP-1 expression. The results of this study suggest that phloroglucinol may be useful as a photoprotective compound for the skin.
Photochemistry and Photobiology 03/2012; 88(2):381-8. · 2.41 Impact Factor
-
Kyoung Ah Kang,
Young Hee Maeng,
Rui Zhang,
Young Ro Yang, Mei Jing Piao,
Ki Cheon Kim,
Gi Young Kim,
Young Ree Kim,
Young Sang Koh,
Hee Kyoung Kang,
Chang Lim Hyun,
Weon Young Chang,
Jin Won Hyun
[show abstract]
[hide abstract]
ABSTRACT: Heme oxygenase-1 (HO-1) catabolizes heme into carbon monoxide, biliverdin, and free iron which mediate its protective effect against oxidative stress. The aim of the present study was to determine the expression level and activity of HO-1 in Korean colon cancer tissues and cell lines. HO-1 protein expression was higher (>1.5-fold) in tumor tissues than in adjacent normal tissues in 14 of 20 colon cancer patients, and HO-1 protein expression was closely correlated with HO-1 enzyme activity in cancer tissues. Immunohistochemical data confirmed that HO-1 protein was expressed at a higher level in colon cancer tissues than in normal mucosa. Furthermore, HO-1 mRNA and protein expression and enzyme activity were higher in the colon cancer cell lines Caco-2, SNU-407, SNU-1033, HT-29, and SW-403 than in the normal fetal human colon cell line FHC. Treatment with the HO-1 inhibitor zinc protoporphyrin decreased the viability of colon cancer cell lines. These data indicate that HO-1 may serve as a clinically useful biomarker of colon cancer and as a target for anticolon cancer drugs.
Tumor Biology 02/2012; 33(4):1031-8. · 1.94 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: In previous reports, the antioxidant effects of eckol were shown to protect cells against hydrogen peroxide- and gamma ray-induced oxidative stress. In this study, the role of eckol in protecting human skin keratinocytes (HaCaT) against UVB-induced oxidative cell damage was investigated. Also, triphlorethol-A, one of the chemical components in Ecklonia cava, and quercetin a well known antioxidant, were compared with eckol in terms of antioxidant activity based on chemical structure. Eckol decreased UVB-induced intracellular reactive oxygen species (ROS), decreased injury to cellular components resulting from UVB-induced oxidative stress, and restored cell viability. In addition, eckol reduced UVB-induced apoptosis by inhibiting the disruption of mitochondrial membranes. These results suggest that eckol protects human keratinocytes against UVB-induced oxidative stress by scavenging ROS, thereby lessening injury to cellular components.
Biological & Pharmaceutical Bulletin 01/2012; 35(6):873-80. · 1.66 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The present study investigated the photoprotective properties of an ethanol extract derived from the red alga Bonnemaisonia hamifera against ultraviolet B (UVB)-induced cell damage in human HaCaT keratinocytes. The Bonnemaisonia hamifera ethanol extract (BHE) scavenged the superoxide anion generated by the xanthine/xanthine oxidase system and the hydroxyl radical generated by the Fenton reaction (FeSO(4) + H(2)O(2)), both of which were detected by using electron spin resonance spectrometry. In addition, BHE exhibited scavenging activity against the 1,1-diphenyl-2-picrylhydrazyl radical and intracellular reactive oxygen species (ROS) that were induced by either hydrogen peroxide or UVB radiation. BHE reduced UVB-induced apoptosis, as shown by decreased apoptotic body formation and DNA fragmentation. BHE also attenuated DNA damage and the elevated levels of 8-isoprostane and protein carbonyls resulting from UVB-mediated oxidative stress. Furthermore, BHE absorbed electromagnetic radiation in the UVB range (280-320 nm). These results suggest that BHE protects human HaCaT keratinocytes against UVB-induced oxidative damage by scavenging ROS and absorbing UVB photons, thereby reducing injury to cellular components.
Marine Drugs 01/2012; 10(12):2826-45. · 3.85 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Oxidative stress is related to the synthesis of matrix metalloproteinases (MMPs), which cause skin aging. The protective effects of mangiferin derived from Anemarrhena asphodeloides were investigated against hydrogen peroxide (H(2)O(2))-induced damage using human skin keratinocyte (HaCaT) cells. Mangiferin was found to scavenge intracellular reactive oxygen species (ROS), superoxide radicals, and hydroxyl radicals. ROS regulate MMPs gene expression and activation of proenzymes. Mangiferin inhibited H(2)O(2)-induced MMP-1 gene expression and protein levels as well as its activity. Moreover, it abrogated mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK) pathway and stress-activated protein kinase/extracellular signal-regulated kinase (SEK)-c-JUN N-terminal kinase (JNK) pathway, which are induced by H(2)O(2) treatment. And, it inhibited DNA binding activity of activator protein-1 (AP-1), a transcription factor of MMP-1 and downstream of ERK and JNK. Finally, it protected the human skin keratinocytes from H(2)O(2)-induced cell death. Taken together, these results indicate that mangiferin attenuated H(2)O(2)-induced MMP-1 activation via inhibition of ERK and JNK pathway and AP-1.
Bioscience Biotechnology and Biochemistry 12/2011; 75(12):2321-5. · 1.28 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Although silver nanoparticles (AgNPs) have been reported to exert strong acute toxic effects on various cultured cells by inducing oxidative stress, the molecular mechanisms by which AgNPs-damaged cells are unknown. Because the endoplasmic reticulum (ER) may play an important role in the response to oxidative stress-induced damage and is quite sensitive to oxidative damage, we hypothesized that AgNPs may exert cytotoxic effects on cells by modulating ER stress. In our study, AgNPs resulted in cytotoxicity and apoptotic cell death when analyzing cell viability, DNA fragmentation and the apoptotic sub-G(1) population. Flow cytometry and confocal microscopy indicated that the cells were sensitive to AgNPs with respect to the induction of mitochondrial Ca(2+) overloading and enhancement of ER stress. AgNPs induced a number of signature ER stress markers, including phosphorylation of RNA-dependent protein kinase-like ER kinase (PERK) and its downstream eukaryotic initiation factor 2α, phosphorylation of inositol-requiring protein 1 (IRE1), splicing of ER stress-specific X-box transcription factor-1, cleavage of activating transcription factor 6 (ATF6) and up-regulation of glucose-regulated protein-78 and CCAAT/enhancer-binding protein-homologous protein (CHOP/GADD153). Down-regulation of PERK, IRE1 and ATF6 expression using siRNA significantly decreased AgNPs-induced the enhancement of ER stress. In addition, down-regulation of CHOP expression with siRNA CHOP attenuated AgNPs-induced apoptosis. Taken together, the present study supports an important role for the ER stress response in mediating AgNPs-induced apoptosis.
The international journal of biochemistry & cell biology 11/2011; 44(1):224-32. · 4.89 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Ultraviolet B (UVB) radiation on human skin induces pathophysiological processes such as oxidative stress and inflammation. In previous reports, the antioxidant effects of triphlorethol-A were shown to protect cells against hydrogen peroxide-induced cell damage and gamma ray-induced oxidative stress. In this study, the role of triphlorethol-A in protecting human keratinocytes (HaCaT) against UVB-induced cell damage was investigated. Triphlorethol-A-treated cells were irradiated with UVB (150 mJ/cm(2)). Triphlorethol-A decreased UVB-induced intracellular ROS and restored the activities of antioxidant enzymes decreased by UVB radiation. Triphlorethol-A decreased UVB damage to cellular components, such as lipid membrane and DNA, restored cell viability and reduced UVB-induced apoptosis by inhibiting the mitochondria-mediated caspase pathway. Triphlorethol-A also reduced the UVB-induced loss of ΔΨ(m) and the active forms of caspase 9 and caspase 3. The anti-apoptotic effect of triphlorethol-A was found to involve the inhibition of c-Jun NH(2)-terminal kinase, which was induced by UVB exposure. And triphlorethol-A showed an absorptive capacity at range of UVB. These results suggest that triphlorethol-A protects human keratinocytes against UVB by enhancing the activities of the antioxidant system, inhibiting cellular damage and absorbing the UVB.
Journal of photochemistry and photobiology. B, Biology 10/2011; 106:74-80. · 1.87 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Baicalein (5,6,7-trihydroxyflavone) is a phenolic flavonoid compound derived mainly from the root of Scutellaria baicalensis Georgi, a medicinal plant traditionally used in oriental medicine. In our previous study, baicalein attenuated mitochondrial oxidative stress by scavenging reactive oxygen species (ROS) and by induction of nuclear factor erythroid 2-related factor 2 transcription factor-mediated manganese superoxide dismutase. In the present study, the protective effects of baicalein against oxidative stress-induced damage, especially cellular components including DNA, lipid, and protein, were studied. The results of this study showed that baicalein scavenged intracellular ROS. Baicalein inhibited the H₂O₂-induced DNA damage that was demonstrated by decreased phospho-H2A.X expression and DNA tail formation. In addition, it prevented the lipid peroxidation shown by the fluorescence intensity of diphenyl-1-pyrenylphosphine and the formation of thiobarbituric acid reactive substances. Moreover, baicalein inhibited protein oxidation demonstrated by protein carbonyl formation. Furthermore, baicalein protected cells via the inhibition of apoptosis induced by H₂O₂. The findings of this study suggest that baicalein provides protection for cellular components against oxidative damage via scavenging ROS and inhibiting apoptosis.
Toxicology and Industrial Health 09/2011; 28(5):412-21. · 1.42 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Recently, we reported that silver nanoparticles (AgNPs) induced reactive oxygen species (ROS) generation and the resultant oxidative stress contributes to the cell damage associated with AgNPs. 8-Oxoguanine (8-oxoG) is sensitive marker of ROS-induced DNA damage. 8-Oxoguanine DNA glycosylase 1 (OGG1) is an important DNA repair enzyme that recognizes and excises 8-oxoG. The aim of the present study was to examine the effect of AgNPs-induced oxidative stress on OGG1 and to elucidate mechanisms underlying AgNPs toxicity. AgNPs decreased OGG1 mRNA and protein expression, resulting in decreased OGG1 activity. Decreased OGG1 activity in AgNPs-treated cells led to increased 8-oxoG levels. The transcription factor NF-E2-related factor 2 (Nrf2) is an important factor in the inducible regulation of OGG1. AgNPs treatment decreased nuclear Nrf2 expression, translocation into nucleus, and transcriptional activity of Nrf2. Extracellular regulated kinase (ERK) and protein kinase B (PKB, AKT), which are upstream of Nrf2, contribute to OGG1 expression. AgNPs attenuated both active forms of ERK and AKT protein expression, resulting in suppression of Nrf2 and decrease of OGG1 expression. These studies demonstrate that down-regulation of Nrf2-mediated OGG1 in exposure to AgNPs occurs through ERK and AKT inactivation.
Toxicology Letters 09/2011; 207(2):143-8. · 3.23 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The radioprotective effect of geraniin, a tannin compound isolated from Nymphaea tetragona Georgi var. (Nymphaeaceae), against γ-radiation-induced damage was investigated in Chinese hamster lung fibroblast (V79-4) cells. Geraniin recovered cell viability detected by MTT test and colony formation assay, which was compromised by γ-radiation, and reduced the γ-radiation-induced apoptosis by the inhibition of loss of the mitochondrial membrane potential. Geraniin protected cellular components (lipid membrane, cellular protein, and DNA) damaged by γ-radiation, which was detected by lipid peroxidation, protein carbonyl formation, and comet assay. Geraniin significantly reduced the level of intracellular reactive oxygen species generated by γ-radiation, which was detected using spectrofluorometer, flow cytometer, and confocal microscope after 2',7'-dichlorodihydrofluorescein diacetate staining. Geraniin normalized the superoxide dismutase and catalase activities, which were decreased by γ-radiation. These results suggest that geraniin protects cells against radiation-induced oxidative stress via enhancing of antioxidant enzyme activities and attenuating of cellular damage.
Cell Biology and Toxicology 04/2011; 27(2):83-94. · 2.51 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Silver nanoparticles (AgNPs), which have well-known antimicrobial properties, are extensively used in various medical and general applications. Despite the widespread use of AgNPs, relatively few studies have been undertaken to determine the cytotoxic effects of AgNPs exposure. This study investigates possible molecular mechanisms underlying the cytotoxic effects of AgNPs. Here, we show that AgNPs-induced cytotoxicity was higher compared than that observed when AgNO(3) was used as a silver ion source. AgNPs induced reactive oxygen species (ROS) generation and suppression of reduced glutathione (GSH) in human Chang liver cells. ROS generated by AgNPs resulted in damage to various cellular components, DNA breaks, lipid membrane peroxidation, and protein carbonylation. Upon AgNPs exposure, cell viability decreased due to apoptosis, as demonstrated by the formation of apoptotic bodies, sub-G(1) hypodiploid cells, and DNA fragmentation. AgNPs induced a mitochondria-dependent apoptotic pathway via modulation of Bax and Bcl-2 expressions, resulting in the disruption of mitochondrial membrane potential (Δψ(m)). Loss of Δψ(m) was followed by cytochrome c release from the mitochondria, resulting in the activation of caspases 9 and 3. The apoptotic effect of AgNPs was exerted via the activation of c-Jun NH(2)-terminal kinase (JNK) and was abrogated by the JNK-specific inhibitor, SP600125 and siRNA targeting JNK. In summary, the results suggest that AgNPs cause cytotoxicity by oxidative stress-induced apoptosis and damage to cellular components.
Toxicology Letters 02/2011; 201(1):92-100. · 3.23 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Formaldehyde (HCHO) generates reactive oxygen species (ROS) that induce DNA base modifications and DNA strand breaks and contributes to mutagenesis and other pathological processes. DNA non-homologous end-joining (NHEJ), a major mechanism for repairing DNA double-stranded breaks (DSB) in mammalian cells, involves the formation of a Ku protein heterodimer and recruitment of a DNA-dependent protein kinase catalytic subunit (DNA-PKcs) to the site of DNA damage. HCHO treatment induced DSB and decreased the protein expressions of Ku 70 and phosphorylated DNA-PKcs. Triphlorethol-A reduced DNA strand breaks and restored the expression of NHEJ-related proteins. In response to oxidative DNA base damage, 8-oxoguanine DNA glycosylase 1 (OGG1) plays a vital role in repair of 8-hydroxy-2'-deoxyguanosine (8-OhdG) via the base-excision repair (BER) process. In this study, HCHO significantly increased 8-OhdG levels, whereas triphlorethol-A lowered 8-OhdG levels. Suppression of 8-OhdG formation by triphlorethol-A was related to enhanced OGG1 protein expression. Triphlorethol-A also enhanced the expression of phosphorylated Akt (the active form of Akt), a regulator of OGG1, which was found to be decreased by HCHO treatment. The phosphoinositol 3-kinase (PI3K)-specific inhibitor LY294002 abolished the cytoprotective effects induced by triphlorethol-A, suggesting that OGG1 restoration by triphlorethol-A is involved in the PI3K/Akt pathway. These results suggest that triphlorethol-A may protect cells against HCHO-induced DNA damage via enhancement of NHEJ and BER capacity.
Journal of Toxicology and Environmental Health Part A 01/2011; 74(12):811-21. · 1.83 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The aim of this study was to investigate the antioxidant properties of the ethanol extract of the flower of Camellia japonica (Camellia extract). Camellia extract exhibited 1,1-diphenyl-2-picrylhydrazyl radical and intracellular reactive oxygen species (ROS) scavenging activity in human HaCaT keratinocytes. In addition, Camellia extract scavenged superoxide anion generated by xanthine/xanthine oxidase and hydroxyl radical generated by the Fenton reaction (FeSO(4) + H(2)O(2)) in a cell-free system, which was detected by electron spin resonance spectrometry. Furthermore, Camellia extract increased the protein expressions and activity of cellular antioxidant enzymes, such as superoxide dismutase, catalase and glutathione peroxidase. These results suggest that Camellia extract exhibits antioxidant properties by scavenging ROS and enhancing antioxidant enzymes. Camellia extract contained quercetin, quercetin-3-O-glucoside, quercitrin and kaempferol, which are antioxidant compounds.
International Journal of Molecular Sciences 01/2011; 12(4):2618-30. · 2.60 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Recently, we demonstrated that butin (7,3',4'-trihydroxydihydroflavone) protected cells against hydrogen peroxide (H(2)O(2))-induced apoptosis by: (1) scavenging reactive oxygen species (ROS), activating antioxidant enzymes such superoxide dismutase and catalase; (2) decreasing oxidative stress-induced 8-hydroxy-2'-deoxyguanosine levels via activation of oxoguanine glycosylase 1, and (3), reducing oxidative stress-induced mitochondrial dysfunction. The objective of this study was to determine the cytoprotective effects of butin on oxidative stress-induced mitochondria-dependent apoptosis, and possible mechanisms involved. Butin significantly reduced H(2)O(2)-induced loss of mitochondrial membrane potential as determined by confocal image analysis and flow cytometry, alterations in Bcl-2 family proteins such as decrease in Bcl-2 expression and increase in Bax and phospho Bcl-2 expression, release of cytochrome c from mitochondria into the cytosol and activation of caspases 9 and 3. Furthermore, the anti-apoptotic effect of butin was exerted via inhibition of mitogen-activated protein kinase kinase-4, c-Jun NH(2)-terminal kinase (JNK) and activator protein-1 cascades induced by H(2)O(2) treatment. Finally, butin exhibited protective effects against H(2)O(2)-induced apoptosis, as demonstrated by decreased apoptotic bodies, sub-G(1) hypodiploid cells and DNA fragmentation. Taken together, the protective effects of butin against H(2)O(2)-induced apoptosis were exerted via blockade of membrane potential depolarization, inhibition of the JNK pathway and mitochondria-involved caspase-dependent apoptotic pathway.
International Journal of Molecular Sciences 01/2011; 12(6):3871-87. · 2.60 Impact Factor
