Cordycepin Attenuates Neointimal Formation by Inhibiting Reactive Oxygen Species–Mediated Responses in Vascular Smooth Muscle Cells in Rats

Won, Kyung‐Jong; Lee, Su-Chan; Lee, Chang-Kwon; Lee, Hwan Myung; Lee, So Hee; Fang, Zhi; Choi, Ok Byung; Jin, Meihua; Kim, Junghwan; Park, Taekyu; Choi, Wahn Soo; Kim, Si-Kwan; Kim, Bokyung

doi:10.1254/jphs.08308fp

Cited by 60 publications

(49 citation statements)

References 34 publications

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“…Natural products, which have been traditionally used in the treatment of inflammatory disease, are considered novel and effective biological agents (10)(11)(12)(13). To develop novel therapeutic agents, it is important to investigate the mechanism regulating inflammatory signal reactions.…”

Section: Discussionmentioning

confidence: 99%

“…Cordyceps spp., whose main chemical constituent is cordycepin, have also been demonstrated to confer anti-inflammatory effects. Won et al reported that cordycepin attenuated neointimal formation by inhibiting reactive oxygen species (ROS)-mediated responses in vascular smooth muscle cells in rats (11). Moreover, some studies have reported that the natural component specifically inhibited the transcriptional activity in the cytokine-stimulated pro-inflammatory response (12,13).…”

Section: Introductionmentioning

confidence: 99%

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The n-butanol fraction of Naematoloma sublateritium suppresses the inflammatory response through downregulation of NF-κB in human endothelial cells

et al. 2012

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Abstract. Naematoloma sublateritium (Fr.) P. Karst is a chestnut mushroom that is currently a popular edible fungus in the USA, Japan, China and Korea. Although its therapeutic potential in the treatment of diseases has been demonstrated, the pharmacological effect of N. sublateritium (NS) has been poorly studied. In the present study, we demonstrate for the first time that NS suppresses TNF-α-induced inflammatory response in human umbilical vein endothelial cells. The n-butanol fraction of NS (BFNS) inhibited TNF-α-induced monocyte adhesion to endothelial cells in a dose-dependent manner. The anti-adhesive activity of BFNS correlated with suppressed expression of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, monocyte chemoattractant protein-1 and interleukin-8 at both the mRNA and protein levels. In addition, BFNS dose-dependently decreased the expression of inducible nitrogen oxygen synthase (iNOS) and cyclooxygenase-2 (COX-2). Notably, BFNS significantly regulated the nuclear factor (NF)-κB transcriptional activity that was activated by TNF-α stimulation. When considered together, these results suggest that BFNS inhibits the expression of TNF-α-induced adhesion molecules in addition to regulating the iNOS/COX-2 pathways through the modulation of NF-κB in endothelial cells. In conclusion, we propose that BFNS may be a potential therapeutic agent against vascular inflammation, such as atherosclerosis. IntroductionAtherosclerosis, a cardiovascular disease, is a leading cause of death worldwide and is the result of a complicated inflammatory processes on the inner wall of large blood vessels. Immune responses can cause vascular endothelial dysfunctions that eventually disturb blood flow (1). In the early pathogenesis of atherosclerosis, the endothelium is activated by a variety of relevant stimuli, including oxidized lipids, cytokines, or signaling molecules such as endotoxins, and viruses, subsequently expressing specific adhesion receptors that enhance mononuclear cell recruitment into the vessel wall (2,3).The immune reactions in atherosclerotic lesions are mediated by nitric oxide (NO) and cyclooxygenase-2 (COX-2) (4). In the physiological function of the endothelium, NO production is required to inhibit monocyte adhesion and smooth muscle cell chemotaxis and proliferation (5). However, high levels of NO, which are produced by inducible NO synthase (iNOS) in response to stimuli, induce subsequent inflammatory reactions, thus contributing to the progression of atherosclerosis (6). COX-2 has also been associated with pro-atherogenic reactions, generating lipid mediators of inflammation, such as prostaglandin E 2 (PGE 2 ) (7).Epidemiological data continue to support the premise that dietary intake of natural products may improve vascular endothelial dysfunction in both in vivo and in vitro atherosclerotic models (8,9). For example, popular and edible mushrooms have been traditionally used to maintain health, and their components have been used in the prevention and treatment of diseases i...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The n-butanol fraction of Naematoloma sublateritium suppresses the inflammatory response through downregulation of NF-κB in human endothelial cells

et al. 2012

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“…Some drugs are also known to contract smooth muscle 2,3) . Many previous studies, including our own, have reported on signal transduction mechanisms and smooth muscle contractions [4][5][6][7][8][9][10][11][12][13][14] . In spite of the importance of the smooth muscle in the fields of cardiovascular physiotherapy, obstetrics, and clinical methods, there is still a need for more research [15][16][17] .…”

Section: Introductionmentioning

confidence: 89%

“…This contraction pathway begins with the activation of GTP-binding proteins by an external stimulus. The external stimulus activates the acceptor resulting in the activation of the α-subunit of trimeric G-protein such as Gα q , Gα 12,13 , and Gα i-2 . The activated Gα-subunit activates Rho guanine nucleotide exchange factor (Rho GEF) 45) .…”

Section: ) Rho-associated Coiled Coil-forming Protein Kinase (Rock) mentioning

confidence: 99%

A Review of Signal Transduction in Mechanisms of Smooth Muscle Contraction and Its Relevance for Specialized Physical Therapy

Kim

Lee

et al. 2013

J Phys Ther Sci

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Abstract.[Purpose] An understanding of smooth muscle contraction is important in the study of specialized physical therapy. In this paper, we summarize the contraction mechanisms of smooth muscle and suggest their applications in physical therapy. [Method] This review focuses on the signaling pathways that control smooth muscle contraction and its mechanisms. We include results reported by our laboratory in a wider literature review. [Results] Our results and the literature show that various mechanisms of smooth muscle contraction exist. [Conclusions] In this review article, we carefully discuss the signal transduction in smooth muscle contraction based on our studies and with reference to physical therapy.

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“…Although some herbal medicines have been used for the prevention or treatment of cardiovascular diseases like atherosclerosis (Mashour et al, 1998), there are no reports of CBMF being used to treat vascular disorders. Since there are many reports about other herbal extracts inhibiting VSMC migration and proliferation that are key events in neointima formation (Choi et al, 2009;Won et al, 2009), we here explored whether CBMF floral water (CBMFF) could affect PDGF-BB-induced proliferation and migration of rat aortic smooth muscle cells (RASMCs).…”

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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Cordycepin Attenuates Neointimal Formation by Inhibiting Reactive Oxygen Species–Mediated Responses in Vascular Smooth Muscle Cells in Rats

Cited by 60 publications

References 34 publications

The n-butanol fraction of Naematoloma sublateritium suppresses the inflammatory response through downregulation of NF-κB in human endothelial cells

The n-butanol fraction of Naematoloma sublateritium suppresses the inflammatory response through downregulation of NF-κB in human endothelial cells

A Review of Signal Transduction in Mechanisms of Smooth Muscle Contraction and Its Relevance for Specialized Physical Therapy

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

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