Photo-protective effect of sargachromenol against UVB radiation-induced damage through modulating cellular antioxidant systems and apoptosis in human keratinocytes

Fernando, Pattage Madushan Dilhara Jayatissa; Piao, Mei Jing; Hewage, Susara Ruwan Kumara Madduma; Kang, Hee Kyoung; Yoo, Eun Sook; Koh, Young Sang; Ko, Mi Hee; Ko, Chang Sik; Byeon, Sang Hee; Mun, Seung Ri; Lee, Nam Ho; Hyun, Jin Won

doi:10.1016/j.etap.2016.02.012

Cited by 17 publications

(13 citation statements)

References 22 publications

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“…2 ). The molecular mechanisms underlying UVB-induced apoptosis are initiated by ROS generation and subsequent oxidative DNA damage resulting in the activation of apoptotic markers [40] . According to the results of the present study, UVB-exposed cells were characterized by the reduced cell viability, formation of apoptotic bodies, reduction of anti-apoptotic protein expression and induction of pro-apoptotic protein expression.…”

Section: Discussionmentioning

confidence: 99%

Juglans regia L. protects against UVB induced apoptosis in human epidermal keratinocytes

Muzaffer

Paul

Prasad

et al. 2018

Biochemistry and Biophysics Reports

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The present study was aimed to investigate the photoprotective effect of the male flower of J. regia L. (MEJR) against ultraviolet-B induced apoptosis in human skin cells. Human skin epidermal keratinocytes were pretreated with the MEJR (80 µg/ml, has been selected after MTT assay), prior to 30 min UVB-irradiation at a dose of 20 mJ/cm2. Mitochondrial membrane potential was evaluated using Rhodamine-123 staining; the % apoptosis by Hoechst staining and acridine orange staining; DNA damage was measured by comet assay. The levels of p53, Bax, Bcl-xL, Bcl-2, Cytochrome c, Caspase-9 and Caspase-3 expression in HaCaT cells were analyzed by western blotting and RT-PCR. Pretreatment with MEJR 80 µg/ml prior to UVB-irradiation significantly prevents apoptotic characteristics, DNA damage and loss of mitochondrial membrane potential. Thus, MEJR protects UVB-mediated human skin cells, by modulating the expression of apoptotic markers and UVB-induced DNA damage in HaCaT cells.

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Section: Discussionmentioning

confidence: 99%

Juglans regia L. protects against UVB induced apoptosis in human epidermal keratinocytes

Muzaffer

Paul

Prasad

et al. 2018

Biochemistry and Biophysics Reports

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“…Sargassum serratifolium C. Agardh (Phaeophyceae, Fucales) possesses anti-tumor [ 36 ] and anti-cancer [ 17 ] activities. Previous phytochemical investigations isolated plastoquinones as secondary metabolites, including sargaquinoic acid, sargahydrogquinoic acid, sargaquinal, and sargachromenol [ 37 ], which possess a wide range of biological activities, including anti-cholinesterase [ 26 ], anti-hyperproliferative disease [ 38 ], neuro-protective [ 39 , 40 ], photo-protective [ 41 ], anti-inflammatory [ 42 , 43 , 44 ], age-related inflammation disease and skin aging protection [ 45 ], anti-diabetic and hypolipidemic [ 46 ], anti-vascular inflammatory [ 19 ], anti-adipogenic [ 47 ], and anti-carcinogenic [ 48 ] properties. Nevertheless, a S. serratifolium preparation has not yet been applied to human health until now, which led us to demonstrate the anti-diabetic potential of S. serratifolium extract and its three major compounds through the inhibition of PTP1B and α-glucosidase.…”

Section: Discussionmentioning

confidence: 99%

α-Glucosidase and Protein Tyrosine Phosphatase 1B Inhibitory Activity of Plastoquinones from Marine Brown Alga Sargassum serratifolium

et al. 2017

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Sargassum serratifolium C. Agardh (Phaeophyceae, Fucales) is a marine brown alga that belongs to the family Sargassaceae. It is widely distributed throughout coastal areas of Korea and Japan. S. serratifolium has been found to contain high concentrations of plastoquinones, which have strong anti-cancer, anti-inflammatory, antioxidant, and neuroprotective activity. This study aims to investigate the anti-diabetic activity of S. serratifolium and its major constituents through inhibition of protein tyrosine phosphatase 1B (PTP1B), α-glucosidase, and ONOO−-mediated albumin nitration. S. serratifolium ethanolic extract and fractions exhibited broad PTP1B and α-glucosidase inhibitory activity (IC50, 1.83~7.04 and 3.16~24.16 µg/mL for PTP1B and α-glucosidase, respectively). In an attempt to identify bioactive compounds, three plastoquinones (sargahydroquinoic acid, sargachromenol and sargaquinoic acid) were isolated from the active n-hexane fraction of S. serratifolium. All three plastoquinones exhibited dose-dependent inhibitory activity against PTP1B in the IC50 range of 5.14–14.15 µM, while sargachromenol and sargaquinoic acid showed dose-dependent inhibitory activity against α-glucosidase (IC50 42.41 ± 3.09 and 96.17 ± 3.48 µM, respectively). In the kinetic study of PTP1B enzyme inhibition, sargahydroquinoic acid and sargaquinoic acid led to mixed-type inhibition, whereas sargachromenol displayed noncompetitive-type inhibition. Moreover, plastoquinones dose-dependently inhibited ONOO−-mediated albumin nitration. Docking simulations of these plastoquinones demonstrated negative binding energies and close proximity to residues in the binding pocket of PTP1B and α-glucosidase, indicating that these plastoquinones have high affinity and tight binding capacity towards the active site of the enzymes. These results demonstrate that S. serratifolium and its major plastoquinones may have the potential as functional food ingredients for the prevention and treatment of type 2 diabetes.

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“…Thus, the proapoptotic JNK cascade ultimately induces apoptosis via the mitochondrial pathway; this apoptotic pathway is also known as the JNK-Bax-caspase-3 pathway [ 45 ]. Previous studies have demonstrated UVB irradiation to activate JNK, as determined by an increase in the phosphorylated form of the enzyme in HCE cells and human keratinocytes [ 9 , 50 , 51 ]. Furthermore, LBPs have been shown to reduce glutamate- and homocysteine-induced phosphorylation of JNK in rat cortical neurons, resulting in a neuroprotective effect [ 41 , 52 ].…”

Section: Discussionmentioning

confidence: 99%

Lycium barbarumPolysaccharides Protect Rat Corneal Epithelial Cells against Ultraviolet B-Induced Apoptosis by Attenuating the Mitochondrial Pathway and Inhibiting JNK Phosphorylation

Han

et al. 2017

BioMed Research International

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Lycium barbarum polysaccharides (LBPs) have been shown to play a key role in protecting the eyes by reducing the apoptosis induced by certain types of damage. However, it is not known whether LBPs can protect damaged corneal cells from apoptosis. Moreover, no reports have focused on the role of LBPs in guarding against ultraviolet B- (UVB-) induced apoptosis. The present study aimed to investigate the protective effect and underlying mechanism of LBPs against UVB-induced apoptosis in rat corneal epithelial (RCE) cells. The results showed that LBPs significantly prevented the loss of cell viability and inhibited cell apoptosis induced by UVB in RCE cells. LBPs also inhibited UVB-induced loss of mitochondrial membrane potential, downregulation of Bcl-2, and upregulation of Bax and caspase-3. Finally, LBPs attenuated the phosphorylation of c-Jun NH2-terminal kinase (JNK) triggered by UVB. In summary, LBPs protect RCE cells against UVB-induced damage and apoptosis, and the underlying mechanism involves the attenuation of the mitochondrial apoptosis pathway and the inhibition of JNK phosphorylation.

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Photo-protective effect of sargachromenol against UVB radiation-induced damage through modulating cellular antioxidant systems and apoptosis in human keratinocytes

Cited by 17 publications

References 22 publications

Juglans regia L. protects against UVB induced apoptosis in human epidermal keratinocytes

Juglans regia L. protects against UVB induced apoptosis in human epidermal keratinocytes

α-Glucosidase and Protein Tyrosine Phosphatase 1B Inhibitory Activity of Plastoquinones from Marine Brown Alga Sargassum serratifolium

Lycium barbarumPolysaccharides Protect Rat Corneal Epithelial Cells against Ultraviolet B-Induced Apoptosis by Attenuating the Mitochondrial Pathway and Inhibiting JNK Phosphorylation

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