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Regression of atherosclerosis by amlodipine via anti-inflammatory and anti-oxidative stress actions.
Hypertens Res. 2006 Jun; 29(6):457-66.HR

Abstract

We examined whether amlodipine, an L-type calcium channel blocker (CCB), has an inhibitory effect on oxidative stress and inflammatory response, and thereby atherosclerosis, in apolipoprotein E-deficient (ApoEKO) mice. Adult male ApoEKO mice (6 weeks of age) were fed a high-cholesterol diet (HCD) for 8 or 10 weeks with or without oral administration of amlodipine (3 mg/kg/day) for 10 weeks or for only the last 2 weeks of the HCD. After HCD feeding, atherosclerotic lesion formation, in situ superoxide production and nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase activity were evaluated in the proximal aorta. The expressions of NADPH oxidase subunits (p47(phox) and rac-1), monocyte chemoattractant protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) were determined with immunohistochemistry and quantitative real-time reverse-transcription polymerase chain reaction. After 8 to 10 weeks of HCD administration to ApoEKO mice, marked atherosclerotic lesion formation was observed in the proximal aorta. In the atherosclerotic lesion, superoxide production, the expression of NADPH oxidase subunits, and NADPH oxidase activity were enhanced, and the expressions of MCP-1, ICAM-1, and VCAM-1 were increased. These changes were suppressed in mice that were treated with amlodipine for 10 weeks concomitant with HCD administration, with no significant change in blood pressure and plasma cholesterol level. We also observed that treatment with amlodipine for only the last 2 weeks regressed the atherosclerotic lesions with a decrease in oxidative stress and vascular inflammation. Inhibition of the atherosclerotic lesion area and lipid area in the proximal aorta by amlodipine was correlated with its inhibitory actions on oxidative stress, inflammation and the production of adhesive molecules. These results suggest that amlodipine not only inhibits atherosclerotic lesion formation, but also regresses atherosclerosis, and that these effects are at least partly due to inhibition of oxidative stress and inflammatory response.

Authors+Show Affiliations

Second Department of Internal Medicine, Ehime University School of Medicine, hitsukawa, Tohon, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16940709

Citation

Yoshii, Toyofumi, et al. "Regression of Atherosclerosis By Amlodipine Via Anti-inflammatory and Anti-oxidative Stress Actions." Hypertension Research : Official Journal of the Japanese Society of Hypertension, vol. 29, no. 6, 2006, pp. 457-66.
Yoshii T, Iwai M, Li Z, et al. Regression of atherosclerosis by amlodipine via anti-inflammatory and anti-oxidative stress actions. Hypertens Res. 2006;29(6):457-66.
Yoshii, T., Iwai, M., Li, Z., Chen, R., Ide, A., Fukunaga, S., Oshita, A., Mogi, M., Higaki, J., & Horiuchi, M. (2006). Regression of atherosclerosis by amlodipine via anti-inflammatory and anti-oxidative stress actions. Hypertension Research : Official Journal of the Japanese Society of Hypertension, 29(6), 457-66.
Yoshii T, et al. Regression of Atherosclerosis By Amlodipine Via Anti-inflammatory and Anti-oxidative Stress Actions. Hypertens Res. 2006;29(6):457-66. PubMed PMID: 16940709.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regression of atherosclerosis by amlodipine via anti-inflammatory and anti-oxidative stress actions. AU - Yoshii,Toyofumi, AU - Iwai,Masaru, AU - Li,Zhen, AU - Chen,Rui, AU - Ide,Ayumi, AU - Fukunaga,Shiori, AU - Oshita,Akira, AU - Mogi,Masaki, AU - Higaki,Jitsuo, AU - Horiuchi,Masatsugu, PY - 2006/8/31/pubmed PY - 2006/9/20/medline PY - 2006/8/31/entrez SP - 457 EP - 66 JF - Hypertension research : official journal of the Japanese Society of Hypertension JO - Hypertens Res VL - 29 IS - 6 N2 - We examined whether amlodipine, an L-type calcium channel blocker (CCB), has an inhibitory effect on oxidative stress and inflammatory response, and thereby atherosclerosis, in apolipoprotein E-deficient (ApoEKO) mice. Adult male ApoEKO mice (6 weeks of age) were fed a high-cholesterol diet (HCD) for 8 or 10 weeks with or without oral administration of amlodipine (3 mg/kg/day) for 10 weeks or for only the last 2 weeks of the HCD. After HCD feeding, atherosclerotic lesion formation, in situ superoxide production and nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase activity were evaluated in the proximal aorta. The expressions of NADPH oxidase subunits (p47(phox) and rac-1), monocyte chemoattractant protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) were determined with immunohistochemistry and quantitative real-time reverse-transcription polymerase chain reaction. After 8 to 10 weeks of HCD administration to ApoEKO mice, marked atherosclerotic lesion formation was observed in the proximal aorta. In the atherosclerotic lesion, superoxide production, the expression of NADPH oxidase subunits, and NADPH oxidase activity were enhanced, and the expressions of MCP-1, ICAM-1, and VCAM-1 were increased. These changes were suppressed in mice that were treated with amlodipine for 10 weeks concomitant with HCD administration, with no significant change in blood pressure and plasma cholesterol level. We also observed that treatment with amlodipine for only the last 2 weeks regressed the atherosclerotic lesions with a decrease in oxidative stress and vascular inflammation. Inhibition of the atherosclerotic lesion area and lipid area in the proximal aorta by amlodipine was correlated with its inhibitory actions on oxidative stress, inflammation and the production of adhesive molecules. These results suggest that amlodipine not only inhibits atherosclerotic lesion formation, but also regresses atherosclerosis, and that these effects are at least partly due to inhibition of oxidative stress and inflammatory response. SN - 0916-9636 UR - https://www.unboundmedicine.com/medline/citation/16940709/Regression_of_atherosclerosis_by_amlodipine_via_anti_inflammatory_and_anti_oxidative_stress_actions_ L2 - https://medlineplus.gov/atherosclerosis.html DB - PRIME DP - Unbound Medicine ER -