scholarly journals Comparative Effects of Biodynes, Tocotrienol-Rich Fraction, and Tocopherol in Enhancing Collagen Synthesis and Inhibiting Collagen Degradation in Stress-Induced Premature Senescence Model of Human Diploid Fibroblasts

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Suzana Makpol ◽  
Faidruz Azura Jam ◽  
Shy Cian Khor ◽  
Zahariah Ismail ◽  
Yasmin Anum Mohd Yusof ◽  
...  
Keyword(s):  
Collagen Synthesis ◽  
Skin Aging ◽  
Collagen Degradation ◽  
Type I ◽  
Premature Senescence ◽  
Diploid Fibroblasts ◽  
Human Diploid Fibroblasts ◽  
Protein Levels ◽  
Stress Induced Premature Senescence ◽  
Tocotrienol Rich Fraction

Biodynes, tocotrienol-rich fraction (TRF), and tocopherol have shown antiaging properties. However, the combined effects of these compounds on skin aging are yet to be investigated. This study aimed to elucidate the skin aging effects of biodynes, TRF, and tocopherol on stress-induced premature senescence (SIPS) model of human diploid fibroblasts (HDFs) by determining the expression of collagen and MMPs at gene and protein levels. Primary HDFs were treated with biodynes, TRF, and tocopherol prior to hydrogen peroxide (H2O2) exposure. The expression ofCOL1A1, COL3A1, MMP1, MMP2, MMP3,andMMP9genes was determined by qRT-PCR. Type I and type III procollagen proteins were measured by Western blotting while the activities of MMPs were quantified by fluorometric Sensolyte MMP Kit. Our results showed that biodynes, TRF, and tocopherol upregulated collagen genes and downregulatedMMPgenes (P<0.05). Type I procollagen and type III procollagen protein levels were significantly increased in response to biodynes, TRF, and tocopherol treatment (P<0.05) with reduction in MMP-1, MMP-2, MMP-3, and MMP-9 activities (P<0.05). These findings indicated that biodynes, TRF, and tocopherol effectively enhanced collagen synthesis and inhibited collagen degradation and therefore may protect the skin from aging.

scholarly journals Inhibition of Mitochondrial CytochromecRelease and Suppression of Caspases by Gamma-Tocotrienol Prevent Apoptosis and Delay Aging in Stress-Induced Premature Senescence of Skin Fibroblasts

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Suzana Makpol ◽  
Norhazira Abdul Rahim ◽  
Chua Kien Hui ◽  
Wan Zurinah Wan Ngah
Keyword(s):  
Caspase 3 ◽  
Annexin V ◽  
Telomerase Activity ◽  
Cellular Aging ◽  
Premature Senescence ◽  
Caspase 9 ◽  
Diploid Fibroblasts ◽  
Human Diploid Fibroblasts ◽  
Apoptotic Effect ◽  
Stress Induced Premature Senescence

In this study, we determined the molecular mechanism ofγ-tocotrienol (GTT) in preventing cellular aging by focusing on its anti-apoptotic effect in stress-induced premature senescence (SIPS) model of human diploid fibroblasts (HDFs). Results obtained showed that SIPS exhibited senescent-phenotypic characteristic, increased expression of senescence-associatedβ-galactosidase (SAβ-gal) and promoted G0/G1cell cycle arrest accompanied by shortening of telomere length with decreased telomerase activity. Both SIPS and senescent HDFs shared similar apoptotic changes such as increased Annexin V-FITC positive cells, increased cytochromecrelease and increased activation of caspase-9 and caspase-3 (P<0.05). GTT treatment resulted in a significant reduction of Annexin V-FITC positive cells, inhibited cytochromecrelease and decreased activation of caspase-9 and caspase-3 (P<0.05). Gene expression analysis showed that GTT treatment down regulated BAX mRNA, up-regulated BCL2A1 mRNA and decreased the ratio of Bax/Bcl-2 protein expression (P<0.05) in SIPS. These findings suggested that GTT inhibits apoptosis by modulating the upstream apoptosis cascade, causing the inhibition of cytochromecrelease from the mitochondria with concomitant suppression of caspase-9 and caspase-3 activation. In conclusion, GTT delays cellular senescence of human diploid fibroblasts through the inhibition of intrinsic mitochondria-mediated pathway which involved the regulation of pro- and anti-apoptotic genes and proteins.

scholarly journals Antiphotoaging Effects of 3,5-Dicaffeoyl-epi-quinic Acid via Inhibition of Matrix Metalloproteinases in UVB-Irradiated Human Keratinocytes

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Jung Hwan Oh ◽  
Jung Im Lee ◽  
Fatih Karadeniz ◽  
So Young Park ◽  
Youngwan Seo ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Quinic Acid ◽  
Human Keratinocytes ◽  
Skin Aging ◽  
Collagen Degradation ◽  
Premature Aging ◽  
Type I ◽  
Dependent Manner ◽  
Protective Effects ◽  
Uvb Irradiation

UVB exposure is one of the causes of several skin complications including but not limited to premature aging, wrinkle formation, and hyperpigmentation. UV-induced skin aging is called photoaging, and oxidative stress-induced overexpression of matrix metalloproteinases (MMPs) is the main reason behind the photoaging-mediated collagen degradation. Natural origin inhibitors of MMPs are regarded as a promising approach to prevent or treat photoaging. Therefore, the present study investigated the protective effects of 3,5-dicaffeoyl-epi-quinic acid (DCEQA) in human HaCaT keratinocytes against UVB irradiation-related dysregulation of MMPs. Changes in the mRNA and protein expression and release of MMP-1, -2, and -9 were observed after UVB irradiation with or without DCEQA treatment. In addition, the effect of DCEQA on the activation of p38, JNK, and ERK MAPKs was analyzed. Treatment of UVB-irradiated HaCaT cells with 10 μM DCEQA significantly suppressed the overexpression of both mRNA and protein of MMP-1, -2, and -9 while slightly increasing the diminished type I procollagen production. UVB-induced activation of MAPKs was also ameliorated by DCEQA treatment in a dose-dependent manner. Results indicated that DCEQA treatment was able to protect keratinocytes from UVB-induced photoaging by inhibiting the stimulated production of MMPs and the related decrease in collagen production. It was suggested that DCEQA downregulated the collagen degradation via inhibition of MAPK activation, which resulted in decreased MMP activity.

scholarly journals Increased abundance of cytoplasmic and nuclear caveolin 1 in human diploid fibroblasts in H2O2-induced premature senescence and interplay with p38αMAPK

FEBS Letters ◽  
2008 ◽  
Vol 582 (12) ◽  
pp. 1685-1692 ◽  
Author(s):  
Aline Chrétien ◽  
Neil Piront ◽  
Edouard Delaive ◽  
Catherine Demazy ◽  
Noëlle Ninane ◽  
...  
Keyword(s):  
Premature Senescence ◽  
Caveolin 1 ◽  
Diploid Fibroblasts ◽  
Human Diploid Fibroblasts

scholarly journals Tocotrienol-Rich Fraction Prevents Cell Cycle Arrest and Elongates Telomere Length in Senescent Human Diploid Fibroblasts

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Suzana Makpol ◽  
Lina Wati Durani ◽  
Kien Hui Chua ◽  
Yasmin Anum Mohd Yusof ◽  
Wan Zurinah Wan Ngah
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Telomere Length ◽  
Telomerase Activity ◽  
S Phase ◽  
Diploid Fibroblasts ◽  
Human Diploid Fibroblasts ◽  
Cycle Arrest ◽  
Tocotrienol Rich Fraction ◽  
Damaged Dna

This study determined the molecular mechanisms of tocotrienol-rich fraction (TRF) in preventing cellular senescence of human diploid fibroblasts (HDFs). Primary culture of HDFs at various passages were incubated with 0.5 mg/mL TRF for 24 h. Telomere shortening with decreased telomerase activity was observed in senescent HDFs while the levels of damaged DNA and number of cells in G0/G1phase were increased and S phase cells were decreased. Incubation with TRF reversed the morphology of senescent HDFs to resemble that of young cells with decreased activity of SA-β-gal, damaged DNA, and cells in G0/G1phase while cells in the S phase were increased. Elongated telomere length and restoration of telomerase activity were observed in TRF-treated senescent HDFs. These findings confirmed the ability of tocotrienol-rich fraction in preventing HDFs cellular ageing by restoring telomere length and telomerase activity, reducing damaged DNA, and reversing cell cycle arrest associated with senescence.

scholarly journals DRG2 Accelerates Senescence via Negative Regulation of SIRT1 in Human Diploid Fibroblasts

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Bing Si Li ◽  
Ai Lin Jin ◽  
ZiQi Zhou ◽  
Jae Ho Seo ◽  
Byung-Min Choi
Keyword(s):  
Oxidative Stress ◽  
Cell Growth ◽  
Binding Protein ◽  
Ectopic Expression ◽  
Sirtuin 1 ◽  
Premature Senescence ◽  
Gtp Binding Protein ◽  
Human Diploid Fibroblasts ◽  
Gtp Binding ◽  
Stress Induced Premature Senescence

Accumulating evidence suggests that developmentally regulated GTP-binding protein 2 (DRG2), an evolutionarily conserved GTP-binding protein, plays an important role in regulating cell growth, inflammation, and mitochondria dynamics. However, the effect of DRG2 in aging remains unclear. In this study, we found that endogenous DRG2 protein expression is upregulated in oxidative stress-induced premature senescence models and tissues of aged mice. Ectopic expression of DRG2 significantly promoted senescence-associated β-galactosidase (SA-β-gal) activity and inhibited cell growth, concomitant with increase in levels of acetyl (ac)-p53 (Lys382), ac-nuclear factor-kB (NF-κB) p65 (Lys310), p21Waf1/Cip1, and p16Ink4a and a decrease in cyclin D1. In this process, reactive oxygen species (ROS) and phosphorylation of H2A histone family member X (H2A.X), forming γ-H2A.X, were enhanced. Mechanistically, ectopic expression of DRG2 downregulated Sirtuin-1 (SIRT1), resulting in augmented acetylation of p53 and NF-κB p65. Additionally, DRG2 knockdown significantly abolished oxidative stress-induced premature senescence. Our results provide a possible molecular mechanism for investigation of cellular senescence and aging regulated by DRG2.

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