Azelnidipine, a new calcium channel blocker, inhibits endothelial inflammatory response by reducing intracellular levels of reactive oxygen species

Naito, Yuji; Shimozawa, Makoto; Manabe, Hikori; Nakabe, Nami; Katada, Kazuhiro; Kokura, Satoshi; Yoshida, Norimasa; Kon, Tatsuya; Yoshikawa, Toshikazu

doi:10.1016/j.ejphar.2006.07.030

Cited by 37 publications

(35 citation statements)

References 30 publications

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“…These actions may be related to AZ's direct scavenging of hydrogen radicals within the cells. In addition, AZ has been shown to suppress the NADPH oxidase expression and activity induced by various stimul (9,11,12,(15)(16)(17)22).…”

Section: Fig 2 the Correlation Between The % Change Of Blood Pressumentioning

confidence: 99%

Combination Therapy with Renin-Angiotensin System Inhibitors and the Calcium Channel Blocker Azelnidipine Decreases Plasma Inflammatory Markers and Urinary Oxidative Stress Markers in Patients with Diabetic Nephropathy

Ogawa¹,

Mori²,

Nako³

et al. 2008

Hypertens Res

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Section: Fig 2 the Correlation Between The % Change Of Blood Pressumentioning

confidence: 99%

Combination Therapy with Renin-Angiotensin System Inhibitors and the Calcium Channel Blocker Azelnidipine Decreases Plasma Inflammatory Markers and Urinary Oxidative Stress Markers in Patients with Diabetic Nephropathy

Ogawa¹,

Mori²,

Nako³

et al. 2008

Hypertens Res

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“…] i was suppressed by KRGE Intracellular calcium elevation is known as a secondary messenger to induce the vascular cell adhesion molecule-1 at the response to the TNF-alpha in the endothelial cells 17,18) . The TNF-alpha (15 ng/ml) significantly increased basal [Ca 2+ ] i compared to the basal state in the endothelial cells.…”

Section: +mentioning

confidence: 99%

Korean Red Ginseng Extract inhibits Tumor Necrosis Factor-alpha-induced Monocyte Adhesion in the Human Endothelial Cells

2008

Journal of Ginseng Research

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Abstracts : Vascular inflammation is an important step in the development of cardiovascular disorder. Since it has not been known whether Korean red ginseng has a role to play on the vascular inflammation, we investigated the effects of Korean red ginseng extract (KRGE) on monocyte adhesion and its underlying signaling mechanism. Monocyte adhesion assay and Western blot were conducted on the human umbilical vein endothelial cells to study monocyte adhesion and the expression of adhesion molecules. Intracellular calcium was measured with Fura-2 fluorescent staining, and superoxide production was measured with lucigenin chemiluminescence in the endothelial cells. KRGE inhibits tumor necrosis factor (TNF)-alpha-induced monocyte adhesion on the endothelial cells at the range of 0.03~1 mg/ml. TNF-alpha-induced vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1 expression were inhibited by the pretreatment of KRGE in the endothelial cells. KRGE also inhibits TNF-alpha-induced intracellular calcium and the superoxide production in the endothelial cells. This study first demonstrated that KRGE inhibits TNF-alpha-induced monocyte adhesion by inhibiting the adhesion molecule expression, intracellular calcium and superoxide production in the endothelial cells. Therefore, the anti-inflammatory function of KRGE may be contributed to protecting the endothelial dysfunction in the vascular inflammatory disorders.

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“…Oxysterols, such as 7-K, 7 -OH and 7 -OH, increase the level of adhesion molecules involved in the recruitment of immunocompetent cells, such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and E-selectin, in HUVECs [43,52,53]. Moreover, incubation with 7-K markedly induces ROS-dependent secretion of VCAM-1 in human aortic endothelial cells 12 (ECs) and U937 cells [54]. It has also been shown that 25-OH can augment eicosanoid release from cultured ECs and increase endothelial-leukocyte interaction by up-regulating VCAM [55].…”

Section: Induction Of the Endothelial Inflammatory Phenotypementioning

confidence: 99%

Inflammation-related gene expression by lipid oxidation-derived products in the progression of atherosclerosis

Leonarduzzi

Gamba

Gargiulo

et al. 2012

Free Radical Biology and Medicine

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Azelnidipine, a new calcium channel blocker, inhibits endothelial inflammatory response by reducing intracellular levels of reactive oxygen species

Cited by 37 publications

References 30 publications

Combination Therapy with Renin-Angiotensin System Inhibitors and the Calcium Channel Blocker Azelnidipine Decreases Plasma Inflammatory Markers and Urinary Oxidative Stress Markers in Patients with Diabetic Nephropathy

Combination Therapy with Renin-Angiotensin System Inhibitors and the Calcium Channel Blocker Azelnidipine Decreases Plasma Inflammatory Markers and Urinary Oxidative Stress Markers in Patients with Diabetic Nephropathy

Korean Red Ginseng Extract inhibits Tumor Necrosis Factor-alpha-induced Monocyte Adhesion in the Human Endothelial Cells

Inflammation-related gene expression by lipid oxidation-derived products in the progression of atherosclerosis

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