(2S)-Naringenin from Typha angustata inhibits vascular smooth muscle cell proliferation via a G0/G1 arrest

Lee, Jung‐Jin; Yi, Hyoseok; Kim, In-Su; Kim, Young S.; Nhiệm, Nguyễn Xuân; Kim, Young Ho; Myung, Chang‐Seon

doi:10.1016/j.jep.2011.12.038

Cited by 26 publications

(21 citation statements)

References 29 publications

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“…Meanwhile, 100 µM naringenin can inhibit angiotensin II-induced proliferation, and migration. These results are consistent with previous studies, 16,17,29) which showed naringenin could inhibit the proliferation of VSMCs stimulated by platelet derived growth factor-BB (PDGF-BB) or tumor necrosis factor (TNF)-α. Yang et al 30) reported that naringenin reduced the binding probability of transforming growth factor beta 1 (TGF-β1) to its specific receptor TβRII, thus inhibiting the receptor dimerization and activation for the signaling complex formation, so it's possible that naringenin inhibited the effects of angiotensin II on VSMCs in the present study by suppressing the binding probability of angiotensin II to AT1 receptor or AT2 receptor and further study is needed. Since others' results combined with our result reveal that naringenin could inhibit VSMCs proliferation and migration induced by different stimulators, naringenin may also affect the critical step of initiation and/or de- velopment of the proliferation and migration of VSMCs.…”

Section: Discussionsupporting

confidence: 93%

“…Since others' results combined with our result reveal that naringenin could inhibit VSMCs proliferation and migration induced by different stimulators, naringenin may also affect the critical step of initiation and/or de- velopment of the proliferation and migration of VSMCs. 16,17,29) Oxidative stress involves the stimulation of VSMCs proliferation and migration 31,32) and plays a critical role in the process of various vascular diseases, such as atherosclerosis and hypertension. 33,34) It is well known that angiotensin II is a vital mediator of oxidative stress and can increase generation of ROS in the vessel wall during the development of these diseases.…”

Section: Discussionmentioning

confidence: 99%

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Naringenin Inhibits Angiotensin II-Induced Vascular Smooth Muscle Cells Proliferation and Migration and Decreases Neointimal Hyperplasia in Balloon Injured Rat Carotid Arteries through Suppressing Oxidative Stress

Chen

Zhang

et al. 2013

Biological & Pharmaceutical Bulletin

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Proliferation and migration of vascular smooth muscle cells (VSMCs) play pivotal roles in the development of restenosis after angioplasty and oxidative stress involves both processes. Naringenin, a flavanone compound found in citrus fruits, has been widely evaluated for antioxidant activity. This study was designed to explore whether naringenin could inhibit angiotensin II-induced VSMCs proliferation and migration and decrease neointimal hyperplasia in balloon injured rat carotid arteries. VSMCs were treated with or without naringenin before stimulation with 1 µM angiotensin II and twenty-four rats were subjected to carotid arteries injury and the carotid arteries were harvested at 14 d after balloon injury. The results showed naringenin led to a significant inhibition of angiotensin II-induced VSMCs proliferation and migration. Naringenin significantly attenuated the reactive oxygen species production, increased the superoxide dismutase activity and decreased the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, reduced phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK) and the nuclear translocation of nuclear factor (NF)-κB p65 in angiotensin II-treated VSMCs. Moreover, naringenin decreased the ratio of neointima to media by 63.8% in balloon injured rat carotid arteries, and the serum level of 8-iso-prostaglandin F2α in naringenin-treated rats was significantly decreased. These results indicated naringenin exhibited antioxidant activity on angiotensin II-treated VSMCs and balloon injured rat carotid arteries and could be a potential protective agent for restenosis after angioplasty.Key words naringenin; vascular smooth muscle cell; oxidative stress; neointimal hyperplasia; angiotensin II Coronary heart disease (CHD) remains the leading cause of mortality in most developed countries and many developing countries.1,2) Percutaneous coronary intervention with or without intracoronary stent placement is widely used for treatment of symptomatic CHD and has greatly improved the survival rate.3,4) However, restenosis after angioplasty, which happen in 5-10% patients, is still a major clinical problem. 5,6) Studies have shown that abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) play pivotal roles in the development of restenosis after angioplasty, as well as in atherosclerosis.7-9) Inhibition of proliferation and migration of VSMCs could remarkably attenuate the neointimal hyperplasia in animal studies. 10-12)Naringenin, a flavanone compound found in citrus fruits, such as oranges and grapes, 13) has been pharmacologically evaluated for antioxidant activity.14,15) Although some studies showed that naringenin could inhibit VSMCs proliferation and migration in vitro, 16,17) the effect and mechanism of naringenin on vascular injury are still far from clear. In this investigation, we attempted to evaluate whether naringenin could inhibit angiotensin II-induced VSMCs proliferation and migration in vitro a...

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Naringenin Inhibits Angiotensin II-Induced Vascular Smooth Muscle Cells Proliferation and Migration and Decreases Neointimal Hyperplasia in Balloon Injured Rat Carotid Arteries through Suppressing Oxidative Stress

Chen

Zhang

et al. 2013

Biological & Pharmaceutical Bulletin

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“…The aortic ring assay revealed that CBMFF attenuated PDGF-BB-induced aortic sprout growth. Migration and proliferation of VSMC participated in the development of atherosclerosis (Lee et al, 2012;Wang et al, 2012). These findings collectively indicate that CBMFF inhibits VSMC migration and proliferation and may regulate vascular disorders such as atherosclerosis.…”

Section: Discussionmentioning

confidence: 66%

“…Vascular smooth muscle cell (VSMC) migration and proliferation are important in the development progression of vascular neointima in atherosclerosis (Lee et al, 2012;Wang et al, 2012). These events were stimulated by various factors, including proinflammatory cytokines and peptide growth factors (Ross, 1999).…”

Section: Introductionmentioning

confidence: 99%

Chrysanthemum borealeflower floral water inhibits platelet-derived growth factor-stimulated migration and proliferation in vascular smooth muscle cells

Kim

Won

Yoon

et al. 2014

Pharmaceutical Biology

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(2015) Chrysanthemumboreale flower floral water inhibits platelet-derived growth factor-stimulated migration and proliferation in vascular smooth muscle cells, Pharmaceutical Biology, 53:5, 725-734, DOI: 10.3109/13880209.2014 Context: Chrysanthemum boreale Makino (Compositae) (CBM) is a traditional medicine that has been used for the prevention or treatment of various disorders; it has various properties including antioxidation, anti-inflammation, and antitumor. Objective: The present study was designed to explore the in vitro effect of CBM flower floral water (CBMFF) on atherosclerosis-related responses in rat aortic smooth muscle cells (RASMCs). Materials and methods: CBMFF was extracted from CBM flower by steam distillation and analyzed using gas chromatography-mass spectrometry. The anti-atherosclerosis activity of CBMFF was tested by estimating platelet-derived growth factor (PDGF)-BB (10 ng/mL)-induced proliferation and migration levels and intracellular kinase pathways in RASMCs at CBMFF concentrations of 0.01-100 lM and analyzing ex vivo aortic ring assay. Results: Gas chromatography-mass spectrometry showed that the CBMFF contained a total of seven components. The CBMFF inhibits PDGF-BB-stimulated RASMC migration and proliferation (IC 50 : 0.010 lg/mL). Treatment of RASMCs with PDGF-BB induced PDGFR-b phosphorylation and increased the phosphorylations of MAPK p38 and ERK1/2. CBMFF addition prevented PDGF-BBinduced phosphorylation of these kinases (IC 50 : 008 and 0.018 lg/mL, for p38 MAPK and ERK1/ 2, respectively), as well as PDGFR-b (IC 50 : 0.046 lg/mL). Treatment with inhibitors of PDGFR, P38 MAPK, and ERK1/2 decreased PDGF-BB-increased migration and proliferation in RASMCs. Moreover, the CBMFF suppressed PDGF-BB-increased sprout outgrowth of aortic rings (IC 50 : 0.047 lg/mL). Discussion and conclusion: These results demonstrate that CBMFF may inhibit PDGF-BB-induced vascular migration and proliferation, most likely through inhibition of the PDGFR-b-mediated MAPK pathway; therefore, the CBMFF may be promising candidate for the development of herbal remedies for vascular disorders.

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“…Notably, the anti-proliferative effect of NRG was associated with the inhibition of DNA synthesis via G0/G1 cell cycle arrest. The cell cycle consists of four sequential phases including G0/G1, S, G2 and M. It regulates cellular proliferation by a highly controlled process involving a complex cascade of cellular events, including regulatory factor cyclins and CDKs (21,22). The cyclin D1-CDK4/6 and cyclin E2-CDK2 complexes are important mediators of the cell cycle transition from the G0/G1 to S-phase (19,20).…”

Section: Discussionmentioning

confidence: 99%

Naringenin inhibits transforming growth factor‑β1‑induced cardiac fibroblast proliferation and collagen synthesis via G0/G1 arrest

Liu

Zhao

et al. 2017

Exp Ther Med

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Abstract. The Traditional Chinese Medicine naringenin (NRG) has a number of biological effects, including anti-inflammatory, anti-oxidative, anti-tumor and anti-atherosclerotic effects. However, the mechanism underlying its effects remains unclear. The aim of the present study is to investigate the role and mechanism of NRG on proliferation and collagen synthesis of cardiac fibroblasts (CFs) induced by transforming growth factor β1 (TGF-β1). Firstly, proliferation and collagen synthesis in CFs subjected to TGF-β1 was assessed subsequent to the consumption of NRG or control treatment. Additionally, the cell cycle of different groups and the roles of cyclins and cyclin-dependent kinases (CDKs) in NRG treatment of CFs were detected. In the present study, it was revealed that treatment of CFs with NRG resulted in attenuated fibroblast α-smooth muscle actin expression, deceased proliferation and collagen synthesis when compared with a TGF-β1 stimulus. Additionally, it was demonstrated that cell population of CFs treated with NRG in the S-phase became smaller whereas that of CFs in the G0/G1-phase increased when compared with the TGF-β1 group. Mechanistically, the expression of cyclin D1-CDK4/6 and cyclin E2-CDK2 were inhibited in the NRG treatment group. These results illustrated that the protective effects of NRG on proliferation and collagen synthesis of CFs were at least in part due to G0/G1 arrest. Therefore, NRG may become a novel strategy for treating cardiac fibrosis in the future.

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(2S)-Naringenin from Typha angustata inhibits vascular smooth muscle cell proliferation via a G0/G1 arrest

Cited by 26 publications

References 29 publications

Naringenin Inhibits Angiotensin II-Induced Vascular Smooth Muscle Cells Proliferation and Migration and Decreases Neointimal Hyperplasia in Balloon Injured Rat Carotid Arteries through Suppressing Oxidative Stress

Naringenin Inhibits Angiotensin II-Induced Vascular Smooth Muscle Cells Proliferation and Migration and Decreases Neointimal Hyperplasia in Balloon Injured Rat Carotid Arteries through Suppressing Oxidative Stress

Chrysanthemum borealeflower floral water inhibits platelet-derived growth factor-stimulated migration and proliferation in vascular smooth muscle cells

Naringenin inhibits transforming growth factor‑β1‑induced cardiac fibroblast proliferation and collagen synthesis via G0/G1 arrest

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