Salidroside protects human fibroblast cells from premature senescence induced by H2O2 partly through modulating oxidative status

Mao, Genxiang; Wang, Yan; Qiu, Qiang; Deng, Hongkui; Yuan, Long-Guo; Li, Ruiguo; Song, Dan–Qing; Li, Yi-yang Yvonne; Li, Dian-Dong; Wang, Zhen

doi:10.1016/j.mad.2010.10.003

Cited by 71 publications

(60 citation statements)

References 39 publications

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“…1A) is an active compound extracted from the root of Rhodiola rosea L that has been used in traditional Tibetan medicine as an adaptogen. This compound is known to possess pharmacological properties including anti-oxidative, neuroprotective and anti-depressive effects [15], [16], [17], [18], [19], [20], [21], [22], [23]. However, the sources of wild Rhodiola rosea L are on the edge of exhaustion.…”

Section: Introductionmentioning

confidence: 99%

Pretreatment with 2-(4-Methoxyphenyl)ethyl-2-acetamido-2-deoxy-β-D-pyranoside Attenuates Cerebral Ischemia/Reperfusion-Induced Injury In Vitro and In Vivo

et al. 2014

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Salidroside, extracted from the root of Rhodiola rosea L, is known for its pharmacological properties, in particular its neuroprotective effects. 2-(4-Methoxyphenyl) ethyl-2-acetamido-2-deoxy-β-D- pyranoside (GlcNAc-Sal), an analog of salidroside, was recently synthesized and shown to possess neuroprotective properties. The purpose of the current study was to investigate the neuroprotective effects of GlcNAc-Sal against oxygen–glucose deprivation-reperfusion (OGD-R)-induced neurotoxicity in vitro and global cerebral ischemia-reperfusion (GCI-R) injury in vivo. Cell viability tests and Hoechst 33342 staining confirmed that GlcNAc-Sal pretreatment markedly attenuated OGD-R induced apoptotic cell death in immortalized mouse hippocampal HT22 cells. Western blot, immunofluorescence and PCR analyses revealed that GlcNAc-Sal pretreatment restored the balance of pro- and anti-apoptotic proteins and inhibited the activation of caspase-3 and PARP induced by OGD-R treatment. Further analyses showed that GlcNAc-Sal pretreatment antagonized reactive oxygen species (ROS) generation, iNOS-derived NO production and NO-related apoptotic cell death during OGD-R stimulation. GCI-R was induced by bilateral common carotid artery occlusion (BCCAO) and reperfusion in mice in vivo. Western blot analysis showed that GlcNAc-Sal pretreatment decreased the expression of caspase-3 and increased the expression of Bcl-2 (B-cell lymphoma 2)/Bax (Bcl-2-associated X protein) induced by GCI-R treatment. Our findings suggest that GlcNAc-Sal pretreatment prevents brain ischemia reperfusion injury by the direct or indirect suppression of cell apoptosis and GlcNAc-Sal could be developed as a broad-spectrum agent for the prevention and/or treatment of cerebral ischemic injury.

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Section: Introductionmentioning

confidence: 99%

Pretreatment with 2-(4-Methoxyphenyl)ethyl-2-acetamido-2-deoxy-β-D-pyranoside Attenuates Cerebral Ischemia/Reperfusion-Induced Injury In Vitro and In Vivo

et al. 2014

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“…It was demonstrated that curcuminoids have potent antioxidative capability, including scavenging free radicals and enhancing antioxidant defense. Since oxidative stress and oxidative stress-induced damage accumulation are important trigger factors of cellular senescence and ageing [4, 5], it is possible that curcuminoids may exert protective roles in the ageing process. Indeed, it has been recently reported that the administration of curcumin could extend the lifespan of two strains of Drosophila melanogaster [6].…”

Section: Introductionmentioning

confidence: 99%

Bisdemethoxycurcumin Increases Sirt1 to Antagonizet-BHP-Induced Premature Senescence in WI38 Fibroblast Cells

Zhong

Chen

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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Curcuminoids are well known for their capabilities to combat risk factors that are associated with ageing and cellular senescence. Recent reports have demonstrated that curcuminoids can extend the lifespan of model organisms. However, the underlying mechanisms by which these polyphenic compounds exert these beneficial effects remain unknown. In this study, t-BHP-induced premature senescence model in human fibroblasts was chosen to explore the protective effects of a curcuminoid, bisdemethoxycurcumin (BDMC), on cellular senescence. The results demonstrated that BDMC attenuated oxidative stress-induced senescence-like features which include the induction of an enlarged cellular appearance, higher frequency of senescence-associated β-galactosidase staining activity, appearance of senescence-associated heterochromatic foci in nuclei, decrease in proliferation capability, and alteration in related molecules such as p16 and retinoblastoma protein. Notably, we found that BDMC treatment activated Sirt1/AMPK signaling pathway. Moreover, downregulating Sirt1 by the pharmacological inhibitor nicotianamine or small interfering RNA blocked BDMC-mediated protection against t-BHP-mediated decrease in proliferation. These results suggested that BDMC prevented t-BHP-induced cellular senescence, and BDMC-induced Sirt1 may be a mechanism mediating its beneficial effects.

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“…Preparations of R. rosea or salidroside protect against oxidative damage caused by hydrogen peroxide in numerous experimental systems involving different cell types, including human neuroblastoma cells (SH-SY5Y and IMR-32) (Zhang et al 2007;Schriner et al 2009), human osteosarcoma cells (Schriner et al 2009), human fetal lung fibroblasts (Mao et al 2010), human hepatocytes (Guan et al 2011b), human cortical neurons (HCN 1-A) (Palumbo et al 2012), human endothelial and endothelial progenitor cells (Xu et al 2013;Zhao et al 2013;Tang et al 2014;Xing et al 2014), rat pheochromocytoma cells (PC12) (Cai et al 2008), primary cultured rat hippocampal and cortical neurons (Chen et al 2009;Shi et al 2012), and rat cardiomyoblasts (H9c2) (Zhu et al 2011). …”

Section: Phytochemical Composition Of Rhodiola Roseamentioning

confidence: 99%

Rhodiola rosea L.: from golden root to green cell factories

et al. 2016

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Salidroside protects human fibroblast cells from premature senescence induced by H2O2 partly through modulating oxidative status

Cited by 71 publications

References 39 publications

Pretreatment with 2-(4-Methoxyphenyl)ethyl-2-acetamido-2-deoxy-β-D-pyranoside Attenuates Cerebral Ischemia/Reperfusion-Induced Injury In Vitro and In Vivo

Pretreatment with 2-(4-Methoxyphenyl)ethyl-2-acetamido-2-deoxy-β-D-pyranoside Attenuates Cerebral Ischemia/Reperfusion-Induced Injury In Vitro and In Vivo

Bisdemethoxycurcumin Increases Sirt1 to Antagonizet-BHP-Induced Premature Senescence in WI38 Fibroblast Cells

Rhodiola rosea L.: from golden root to green cell factories

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