Fullerenol Protects Retinal Pigment Epithelial Cells From Oxidative Stress–Induced Premature Senescence via Activating SIRT1

Zhuge, Chun-Chun; Xu, Jingying; Zhang, Jingfa; Li, Weiye; Li, Peng; Li, Zongyi; Chen, Ling; Liu, Xiaoqing; Shang, Peng; Xu, Hua; Lu, Yi; Wang, Fang; Lü, Lixia; Xu, Guo‐Tong

doi:10.1167/iovs.13-13732

Cited by 53 publications

(47 citation statements)

References 37 publications

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“…The agent was shown to induce apoptosis in such cancer cells as skin cancer cells, 35) colon cancer cells, 36) and neuroblastoma Cells, 37) whereas was indicated to exert the protective role against apoptosis in the human tenocytes, 38) in endothelial cells 39) and in other types of cells, 40) particularly, under the pressure of oxidative stress. [40][41][42] And in this study, we confirmed the protective role of RSV and the Sirt 1 activation against the H 2 O 2 -induced apoptosis in MC3T3-E1 osteoblast cells. Moreover, based on the above results, we speculated that activation of p53 acetylation by H 2 O 2 -induced downregulation of Sirt 1 could increase the Bax, whereas could reduce the Bcl-2, at protein level.…”

Section: Discussionsupporting

confidence: 80%

Resveratrol inhibits the hydrogen dioxide-induced apoptosis via Sirt 1 activation in osteoblast cells

Zhu

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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Sirt 1 plays a critical role in stress responses. We determined the deregulation of Sirt 1 activity, p53 acetylation, Bcl-2 expression, and mitochondria-dependent apoptosis in mouse osteoblast MC3T3-E1 cells which were exposed to H2O2. And then we investigated the protective role of Sirt 1 activator, Resveratrol (RSV), against the H2O2-induced apoptosis. Results demonstrated that Sirt 1 and Bcl-2 were inhibited, whereas p53 acetylation, Bax, and caspase 9 were promoted by H2O2, as was aggravated by the Sirt 1 inhibitor, EX-527. Instead, RSV inhibited the H2O2-induced both p53 acetylation and the caspase 9 activation, whereas ameliorated the H2O2-induced Bcl-2 inhibition and apoptosis. In conclusion, Sirt 1 was downregulated during the H2O2-induced apoptosis in MC3T3-E1 cells. And the chemical activation of Sirt 1 inhibited the H2O2-induced apoptosis via the downregulation of p53 acetylation. Our results suggest that Sirt 1 upregulation appears to be an important strategy to inhibit the oxidative stress-induced apoptosis.

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Section: Discussionsupporting

confidence: 80%

Resveratrol inhibits the hydrogen dioxide-induced apoptosis via Sirt 1 activation in osteoblast cells

Zhu

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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“…24,25) The whole cell extracts were incubated with 10 µL SIRT1 Substrate Solution in 96-well plates at 37°C for 30 min, and then mixed with Developing Solution at 37°C for 10 min. Meanwhile, the standard curve was determined.…”

Section: Methodsmentioning

confidence: 99%

Curcumin Attenuates Hydrogen Peroxide-Induced Premature Senescence <i>via</i> the Activation of SIRT1 in Human Umbilical Vein Endothelial Cells

Sun

et al. 2015

Biological & Pharmaceutical Bulletin

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Endothelial senescence has been proposed to be involved in endothelial dysfunction and atherogenesis. Curcumin, a natural phenol, possesses antioxidant and anti-inflammatory properties. However, the effect of curcumin on endothelial senescence is unclear. This study explores the effect of curcumin on hydrogen peroxide (H 2 O 2 )-induced endothelial premature senescence and the mechanisms involved. Human umbilical vein endothelial cells (HUVECs) were cultured, and premature senescence was induced with 100 µM H 2 O 2 . Results showed that pretreatment with curcumin significantly attenuated the H 2 O 2 -induced HUVECs' premature senescence, which was evidenced by a decreased percentage of senescence-associated β-galactosidase positive cells, improved cell division and decreased expression of senescence-associated protein p21 (all p<0.05). Pretreatment with curcumin decreased oxidative stress and apoptosis in H 2 O 2 -treated HUVECs. Treatment of HUVECs with H 2 O 2 also down-regulated the phosphorylation of endothelial nitric oxide synthase (eNOS), decreased the level of nitric oxide in the culture medium, and inhibited the protein expression and enzymatic activity of silent information regulator 1 (SIRT1), while pretreatment with curcumin partly reversed these effects (all p<0.05). Treatment with curcumin alone enhanced the enzymatic activity of SIRT1, but didn't affect cellular senescence, cell growth or apoptosis compared to the Control. The inhibition of SIRT1 using SIRT1 short interfering RNA (siRNA) could decrease the expression and phosphorylation of eNOS and abrogate the protective effect of curcumin on H 2 O 2 -induced premature senescence. These findings suggest that curcumin could attenuate oxidative stress-induced HUVECs' premature senescence via the activation of SIRT1.Key words curcumin; endothelial senescence; silent information regulator 1 (SIRT1); hydrogen peroxide Cellular senescence is defined as an irreversible state of growth arrest and accompanied by a specific set of phenotypic changes, gene expression and cell function.1) It has been realized that senescence is induced by a variety of insults, including those causing intracellular oxidative stress, such as hydrogen peroxide (H 2 O 2 ).2) This kind of cellular senescence is called the stress-induced premature senescence (SIPS). Endothelial senescence has been proposed to be involved in endothelial dysfunction and atherogenesis.3) Human studies showed that there were vascular cells exhibiting the morphological features of cellular senescence. [4][5][6] Silent information regulator 1 (SIRT1) is a member of the sirtuin family of proteins, which are homologs of the Sir2 gene in Saccharomyces (S.) cerevisiae. SIRT1 has been known as an oxidized form of nicotinamide adenine dinucleotide (NAD + )-dependent class III histone deacetylase (HDAC) and plays a key role in regulating cellular senescence, cell survival and metabolism through deacetylation of various histones and non-histone substrates.7,8) SIRT1 is highly expressed in the vasculature. A gro...

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“…23 We used Western blot analysis to evaluate acetyl-p53 expression at 24 and 48 h after TCDD exposure, to assess the possible role of H2 in suppressing cellular senescence. Total p53 expression in HUVECs did not significantly differ between normal and hydrogen-rich media or between media with and without TCDD (Figures 5A,B).…”

Section: Effects Of Hydrogen-rich Medium On P53 Acetylationmentioning

confidence: 99%

“…32, 33 Furthermore, activation of p53 by acetylation was found to be associated with cellular senescence caused by oxidative stress. 23 To examine further the effects of H2 on preventing cellular senescence, we assessed induction of acetyl-p53 in HUVECs treated with hydrogen-rich water. H2 significantly decreased induction of acetyl-p53 at 24 h after TCDD incubation.…”

Section: Effects Of Chrysin On H2-induced Changes In Huvecsmentioning

confidence: 99%

Molecular Hydrogen Alleviates Cellular Senescence in Endothelial Cells

Hara

Tatebe

Watanabe

et al. 2016

Circ J

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Fullerenol Protects Retinal Pigment Epithelial Cells From Oxidative Stress–Induced Premature Senescence via Activating SIRT1

Abstract: Fullerenol could rescue RPE cells from oxidative stress-induced senescence through its antioxidation activity and the activation of SIRT1. The protective effect of Fol is useful for the development of new strategies to treat oxidative stress-related retinal diseases like AMD.

Cited by 53 publications

References 37 publications

Resveratrol inhibits the hydrogen dioxide-induced apoptosis via Sirt 1 activation in osteoblast cells

Resveratrol inhibits the hydrogen dioxide-induced apoptosis via Sirt 1 activation in osteoblast cells

Curcumin Attenuates Hydrogen Peroxide-Induced Premature Senescence <i>via</i> the Activation of SIRT1 in Human Umbilical Vein Endothelial Cells

Molecular Hydrogen Alleviates Cellular Senescence in Endothelial Cells

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