Ionizing Radiation to Prevent Arterial Intimal Hyperplasia At the Edges of the Stent: Induces Necrosis and Fibrosis

Ducasse, Éric; Chevalier, Jacques; Cosset, Jean‐Marc; Creusy, Colette; Eschwège, F.; Speziale, Francesco; Sbarigia, Enrico; Midy, D.; Jc, Baste; Lartigau, Éric

doi:10.1016/j.jss.2006.03.043

Cited by 2 publications

(1 citation statement)

References 29 publications

(46 reference statements)

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“…The medial and intimal thicknesses and areas were measured by image processing software, and the intima/media thicknesses and area ratios were determined. 43 …”

Section: Methodsmentioning

confidence: 99%

Anti-inflammatory effects of a Chinese herbal medicine in atherosclerosis via estrogen receptor β mediating nitric oxide production and NF-κB suppression in endothelial cells

Wang

Qin

et al. 2013

Cell Death Dis

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Bu-Shen-Ning-Xin Decoction (BSNXD) administration has alleviated the early pathologic damage of atherosclerosis by inhibiting the adhesion molecule expression and upregulating the estrogen receptor (ER) β expression in endothelial cells, and increasing the serum nitric oxide (NO) level without any effect on serum lipid status, endometrium and fat deposition in liver in ovariectomized rabbits. The BSNXD-derived serum increases ER β expression in the human umbilical vein endothelial cells (HUVECs), and decreases malondialdehyde (MDA) production, and upregulates eNOS expression then increases NO synthesis through ERβ-dependent pathway. NO not only suppresses the LPS-induced NF-κB transcription in HUVECs, but also decreases apoptosis of endothelial cells. The BSNXD-derived serum decreases monocyte chemoattractant protein-1 production, and suppresses cell adhesion molecules (ICAM-1, VCAM-1 and E-selectin) expression in HUVECs injured by oxidized low-density lipoproteins (ox-LDL), and these effects can be abolished by ERβ antagonist (R,RTHC) and NO synthase inhibitor (L-NAME). The BSNXD-derived serum-treated HUVECs supernatant reduces CCR2, LFA-1 and VLA-4 expression in monocytes cell line U937 cells, which in turn inhibits adherence of U937 to injured endothelial cells. NO synthesis increases, and MDA production decreases through ERβ-mediated pathway that suppresses apoptosis and NF-κB activity in endothelial cells that downregulates adhesion molecules expression on endothelial cells via ERβ/NO/NF-κB pathway, and in turn leukocyte adhesion, which suggests BSNXD potential value in prophylaxis atherosclerosis.

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“…The medial and intimal thicknesses and areas were measured by image processing software, and the intima/media thicknesses and area ratios were determined. 43 …”

Section: Methodsmentioning

confidence: 99%

Anti-inflammatory effects of a Chinese herbal medicine in atherosclerosis via estrogen receptor β mediating nitric oxide production and NF-κB suppression in endothelial cells

Wang

Qin

et al. 2013

Cell Death Dis

View full text Add to dashboard Cite

show abstract

Protective effects of dehydroepiandrosterone on atherosclerosis in ovariectomized rabbits via alleviating inflammatory injury in endothelial cells

Hao

Wang

et al. 2011

Atherosclerosis

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Ionizing Radiation to Prevent Arterial Intimal Hyperplasia At the Edges of the Stent: Induces Necrosis and Fibrosis

Cited by 2 publications

References 29 publications

Anti-inflammatory effects of a Chinese herbal medicine in atherosclerosis via estrogen receptor β mediating nitric oxide production and NF-κB suppression in endothelial cells

Anti-inflammatory effects of a Chinese herbal medicine in atherosclerosis via estrogen receptor β mediating nitric oxide production and NF-κB suppression in endothelial cells

Protective effects of dehydroepiandrosterone on atherosclerosis in ovariectomized rabbits via alleviating inflammatory injury in endothelial cells

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