Rb1 Protects Endothelial Cells from Hydrogen Peroxide-Induced Cell Senescence by Modulating Redox Status

Liu, Dinghui; Chen, Yanming; Liu, Yong; Hao, Baoshun; Zhou, Bin; Wu, Lin; Wang, Min; Chen, Lin; Wu, Weikang; Qian, Xiaoxian

doi:10.1248/bpb.34.1072

Cited by 28 publications

(29 citation statements)

References 30 publications

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“…In our previous study, we found that 20 µmol/L of Rb1 could effectively prevent HUVECs from senescence [11]. As such, we continued to use 20 µmol/L of Rb1 in this study in order to explore its effect.…”

Section: Resultsmentioning

confidence: 96%

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Ginsenoside Rb1 Prevents H2O2-Induced HUVEC Senescence by Stimulating Sirtuin-1 Pathway

et al. 2014

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PurposesWe have previously reported that Ginsenoside Rb1 may effectively prevent HUVECs from senescence, however, the detailed mechanism has not demonstrated up to now. Recent studies have shown that sirtuin-1 (Sirt1) plays an important role in the development of endothelial senescence. The purpose of this study was to explore whether Sirt1 is involved in the action of Ginsenoside Rb1 regarding protection against H2O2-induced HUVEC Senescence.Methods and ResultsSenescence induced by hydrogen peroxide (H2O2) in human umbilical vein endothelial cells (HUVECs) was examined by analyzing plasminogen activator inhibitor-1 (PAI-1) expression, cell morphology, and senescence-associated beta-galactosidase (SA-β-gal) activity. The results revealed that 42% of control-treated HUVECs were SA-β-gal positive after treatment by 60 µmol/L H2O2, however, this particular effect of H2O2 was decreased more than 2-fold (19%) in the HUVECs when pretreated with Rb1 (20 µmol/L) for 30 min. Additionally, Rb1 decreased eNOS acetylation, as well as promoted more NO production that was accompanied by an increase in Sirt1 expression. Furthermore, upon knocking down Sirt1, the effect of Rb1 on HUVEC senescence was blunted.ConclusionsThe present study indicated that Ginsenoside Rb1 acts through stimulating Sirt1 in order to protect against endothelial senescence and dysfunction. As such, Sirt1 appears to be of particular importance in maintaining endothelial functions and delaying vascular aging.

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Section: Resultsmentioning

confidence: 96%

“…Our previous studies have shown that Rb1 prevented HUVEC senescence through modulating redox status [11]. However, it is unknown whether Sirt1 is involved in Rb1 prevention of H 2 O 2 -induced HUVEC senescence.…”

Section: Introductionmentioning

confidence: 98%

Ginsenoside Rb1 Prevents H2O2-Induced HUVEC Senescence by Stimulating Sirtuin-1 Pathway

et al. 2014

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“…Recent evidence has indicated that SOCE can be regulated by reactive oxygen species (ROS) through redox-dependent modification of STIM and Orai proteins [57]. Since ginsenoside Rb1 is known to reduce oxidative stress in different cells and tissues [17,27,58,59], it is possible that it modulates SOCE through a ROS-related mechanism.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have shown that vasoreactivity to agonists such as ET-1, 5-HT and Ang II are enhanced in PAs of different PH rat and mouse models [27,28,29,30,31,32,33]. We have recently shown that the enhanced vasoreactivity to ET-1 in PAs of MCT-treated rats is related to the upregulation of store-operated Ca 2+ entry (SOCE).…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rb1 Attenuates Agonist-Induced Contractile Response via Inhibition of Store-Operated Calcium Entry in Pulmonary Arteries of Normal and Pulmonary Hypertensive Rats

Wang

Jiao

et al. 2015

Cell Physiol Biochem

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Background: Pulmonary hypertension (PH) is characterized by sustained vasoconstriction, enhanced vasoreactivity and vascular remodeling, which leads to right heart failure and death. Despite several treatments are available, many forms of PH are still incurable. Ginsenoside Rb1, a principle active ingredient of Panax ginseng, exhibits multiple pharmacological effects on cardiovascular system, and suppresses monocrotaline (MCT)-induced right heart hypertrophy. However, its effect on the pulmonary vascular functions related to PH is unknown. Methods: We examined the vasorelaxing effects of ginsenoside Rb1 on endothelin-1 (ET-1) induced contraction of pulmonary arteries (PAs) and store-operated Ca²⁺ entry (SOCE) in pulmonary arterial smooth muscle cells (PASMCs) from chronic hypoxia (CH) and MCT-induced PH. Results: Ginsenoside Rb1 elicited concentration-dependent relaxation of ET-1-induced PA contraction. The vasorelaxing effect was unaffected by nifedipine, but abolished by the SOCE blocker Gd³⁺. Ginsenoside Rb1 suppressed cyclopiazonic acid (CPA)-induced PA contraction, and CPA-activated cation entry and Ca²⁺ transient in PASMCs. ET-1 and CPA-induced contraction, and CPA-activated cation entry and Ca²⁺ transients were enhanced in PA and PASMCs of CH and MCT-treated rats; the enhanced responses were abolished by ginsenoside Rb1. Conclusion: Ginsenoside Rb1 attenuates ET-1-induced contractile response via inhibition of SOCE, and it can effectively antagonize the enhanced pulmonary vasoreactivity in PH.

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“…NOX oxidizes NADPH to NADP + with the concomitant generation of peroxides, including H 2 O 2 [32]. In contrast, SOD serves as a crucial anti-oxidant enzyme that plays an important role in scavenging oxygen free radicals and protecting tissue from ROS-induced oxidative stress injury [33]. Under normal circumstances, NOX and SOD are maintained in dynamic balance, as the excessive activation of NOX and consumption of SOD synergistically stimulate ROS generation.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Attenuates Oxidative Stress Induced by Balloon Injury in the Rat Carotid Artery Through Actions on the ERK1/2 and NF-Kappa B Pathway

Zhang

Chen

Yang

et al. 2013

Cell Physiol Biochem

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Background/Aim: Oxidative stress plays a critical role in pathogenesis of the neointimal arterial hyperplasia. The aim of the study was to evaluate effects of resveratrol (RSV) on the vascular hyperplasia stimulated by oxidative damage. Methods: Balloon vascular injury was induced in rats that were intraperitonealy exposed to resveratrol (1 mg/kg) on 7 or 14 days after surgical procedure. Animals were euthanized on 7 or 14 days after operation. The blood level of 8-iso-prostaglandin F2α, arterial morphology as well as expression of monocyte chemotactic protein-1 and interleukin-6 in carotid wall were measured. Vascular smooth muscle cells (VSMCs) were isolated from the thoracic aorta. Cellular proliferation and migration assays, reactive oxygen species (ROS), superoxide dismutase (SOD) and NADPH oxidative activity, protein level of β-actin, histone H3, NF-ĸB p65, IĸB, ERK1/2, phospho-ERK1/2, phospho-p38 as well as NF-ĸB transcription activity were evaluated in-vitro after angiotensin II stimulation and resveratrol (50-200 µmol/L) treatment. Results: Significant decreases in neointimal/medial area, serum prostaglandin level and genes expression were found in rats treated with resveratrol, when compared to the control group. Significant changes were also revealed for proliferation and migration rates, ROS level, as well as SOD, NADPH oxidase, ERK1/2 phosphorylation and NF-ĸB transcriptional activity in cell cultures exposed to highest dose of resveratrol. Insignificant changes were observed for NF-kappaB p65 translocation and IĸB degradation, p38 phosphorylation in MAPK pathway. Conclusion: Resveratrol significantly suppressed the neointimal hyperplasia after balloon injury through inhibition of oxidative stress and inflammation by blocking the ERK1/2/NF-kappa B pathway.

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Rb1 Protects Endothelial Cells from Hydrogen Peroxide-Induced Cell Senescence by Modulating Redox Status

Cited by 28 publications

References 30 publications

Ginsenoside Rb1 Prevents H2O2-Induced HUVEC Senescence by Stimulating Sirtuin-1 Pathway

Ginsenoside Rb1 Prevents H2O2-Induced HUVEC Senescence by Stimulating Sirtuin-1 Pathway

Ginsenoside Rb1 Attenuates Agonist-Induced Contractile Response via Inhibition of Store-Operated Calcium Entry in Pulmonary Arteries of Normal and Pulmonary Hypertensive Rats

Resveratrol Attenuates Oxidative Stress Induced by Balloon Injury in the Rat Carotid Artery Through Actions on the ERK1/2 and NF-Kappa B Pathway

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