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Olmesartan, an AT1 antagonist, attenuates oxidative stress, endoplasmic reticulum stress and cardiac inflammatory mediators in rats with heart failure induced by experimental autoimmune myocarditis.
Int J Biol Sci. 2011 Feb 11; 7(2):154-67.IJ

Abstract

Studies have demonstrated that angiotensin II has been involved in immune and inflammatory responses which might contribute to the pathogenesis of immune-mediated diseases. Recent evidence suggests that oxidative stress may play a role in myocarditis. Here, we investigated whether olmesartan, an AT(1)R antagonist protects against experimental autoimmune myocarditis (EAM) by suppression of oxidative stress, endoplasmic reticulum (ER) stress and inflammatory cytokines. EAM was induced in Lewis rats by immunization with porcine cardiac myosin, were divided into two groups and treated with either olmesartan (10 mg/kg/day) or vehicle for a period of 21 days. Myocardial functional parameters measured by hemodynamic and echocardiographic analyses were significantly improved by the treatment with olmesartan compared with those of vehicle-treated rats. Treatment with olmesartan attenuated the myocardial mRNA expressions of proinflammatory cytokines, [Interleukin (IL)-1β, monocyte chemoattractant protein-1, tumor necrosis factor-α and interferon-γ)] and the protein expression of tumor necrosis factor-α compared with that of vehicle-treated rats. Myocardial protein expressions of AT(1)R, NADPH oxidase subunits (p47phox, p67phox, gp91phox) and the expression of markers of oxidative stress (3-nitrotyrosine and 4-hydroxy-2-nonenal), and the cardiac apoptosis were also significantly decreased by the treatment with olmesartan compared with those of vehicle-treated rats. Furthermore, olmesartan treatment down-regulated the myocardial expressions of glucose regulated protein-78, growth arrest and DNA damage-inducible gene, caspase-12, phospho-p38 mitogen-activated protein kinase (MAPK) and phospho-JNK. These findings suggest that olmesartan protects against EAM in rats, at least in part via suppression of oxidative stress, ER stress and inflammatory cytokines.

Authors+Show Affiliations

Department of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, Japan. svkumar1979@yahoo.comNo 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
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21383952

Citation

Sukumaran, Vijayakumar, et al. "Olmesartan, an AT1 Antagonist, Attenuates Oxidative Stress, Endoplasmic Reticulum Stress and Cardiac Inflammatory Mediators in Rats With Heart Failure Induced By Experimental Autoimmune Myocarditis." International Journal of Biological Sciences, vol. 7, no. 2, 2011, pp. 154-67.
Sukumaran V, Watanabe K, Veeraveedu PT, et al. Olmesartan, an AT1 antagonist, attenuates oxidative stress, endoplasmic reticulum stress and cardiac inflammatory mediators in rats with heart failure induced by experimental autoimmune myocarditis. Int J Biol Sci. 2011;7(2):154-67.
Sukumaran, V., Watanabe, K., Veeraveedu, P. T., Gurusamy, N., Ma, M., Thandavarayan, R. A., Lakshmanan, A. P., Yamaguchi, K., Suzuki, K., & Kodama, M. (2011). Olmesartan, an AT1 antagonist, attenuates oxidative stress, endoplasmic reticulum stress and cardiac inflammatory mediators in rats with heart failure induced by experimental autoimmune myocarditis. International Journal of Biological Sciences, 7(2), 154-67.
Sukumaran V, et al. Olmesartan, an AT1 Antagonist, Attenuates Oxidative Stress, Endoplasmic Reticulum Stress and Cardiac Inflammatory Mediators in Rats With Heart Failure Induced By Experimental Autoimmune Myocarditis. Int J Biol Sci. 2011 Feb 11;7(2):154-67. PubMed PMID: 21383952.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Olmesartan, an AT1 antagonist, attenuates oxidative stress, endoplasmic reticulum stress and cardiac inflammatory mediators in rats with heart failure induced by experimental autoimmune myocarditis. AU - Sukumaran,Vijayakumar, AU - Watanabe,Kenichi, AU - Veeraveedu,Punniyakoti T, AU - Gurusamy,Narasimman, AU - Ma,Meilei, AU - Thandavarayan,Rajarajan A, AU - Lakshmanan,Arun Prasath, AU - Yamaguchi,Ken'ichi, AU - Suzuki,Kenji, AU - Kodama,Makoto, Y1 - 2011/02/11/ PY - 2010/09/20/received PY - 2011/02/07/accepted PY - 2011/3/9/entrez PY - 2011/3/9/pubmed PY - 2011/6/9/medline KW - Experimental autoimmune myocarditis KW - endoplasmic reticulum stress KW - inflammation KW - olmesartan KW - oxidative stress SP - 154 EP - 67 JF - International journal of biological sciences JO - Int J Biol Sci VL - 7 IS - 2 N2 - Studies have demonstrated that angiotensin II has been involved in immune and inflammatory responses which might contribute to the pathogenesis of immune-mediated diseases. Recent evidence suggests that oxidative stress may play a role in myocarditis. Here, we investigated whether olmesartan, an AT(1)R antagonist protects against experimental autoimmune myocarditis (EAM) by suppression of oxidative stress, endoplasmic reticulum (ER) stress and inflammatory cytokines. EAM was induced in Lewis rats by immunization with porcine cardiac myosin, were divided into two groups and treated with either olmesartan (10 mg/kg/day) or vehicle for a period of 21 days. Myocardial functional parameters measured by hemodynamic and echocardiographic analyses were significantly improved by the treatment with olmesartan compared with those of vehicle-treated rats. Treatment with olmesartan attenuated the myocardial mRNA expressions of proinflammatory cytokines, [Interleukin (IL)-1β, monocyte chemoattractant protein-1, tumor necrosis factor-α and interferon-γ)] and the protein expression of tumor necrosis factor-α compared with that of vehicle-treated rats. Myocardial protein expressions of AT(1)R, NADPH oxidase subunits (p47phox, p67phox, gp91phox) and the expression of markers of oxidative stress (3-nitrotyrosine and 4-hydroxy-2-nonenal), and the cardiac apoptosis were also significantly decreased by the treatment with olmesartan compared with those of vehicle-treated rats. Furthermore, olmesartan treatment down-regulated the myocardial expressions of glucose regulated protein-78, growth arrest and DNA damage-inducible gene, caspase-12, phospho-p38 mitogen-activated protein kinase (MAPK) and phospho-JNK. These findings suggest that olmesartan protects against EAM in rats, at least in part via suppression of oxidative stress, ER stress and inflammatory cytokines. SN - 1449-2288 UR - https://www.unboundmedicine.com/medline/citation/21383952/Olmesartan_an_AT1_antagonist_attenuates_oxidative_stress_endoplasmic_reticulum_stress_and_cardiac_inflammatory_mediators_in_rats_with_heart_failure_induced_by_experimental_autoimmune_myocarditis_ L2 - https://www.ijbs.com/v07p0154.htm DB - PRIME DP - Unbound Medicine ER -