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Telmisartan ameliorates experimental autoimmune myocarditis associated with inhibition of inflammation and oxidative stress.
Eur J Pharmacol. 2011 Feb 10; 652(1-3):126-35.EJ

Abstract

Excess cytokine produced by inflammatory stimuli contributes to the progression of myocardial damage in myocarditis. Angiotensin-II has been shown to play a pivotal role in the pathophysiology of various organs, especially the cardiovascular system. Some angiotensin II type 1 receptor antagonists are reported to inhibit proinflammatory cytokine production in vitro and in vivo. We investigated whether telmisartan, an angiotensin II type 1 receptor antagonist protects against experimental autoimmune myocarditis by suppression of inflammatory cytokines and oxidative stress. Experimental autoimmune myocarditis was induced in Lewis rats by immunization with porcine cardiac myosin. The rats were divided into two groups and treated with either telmisartan (10mg/kg/day) or vehicle for 21days. Age-matched normal rats without immunization were also included in this study. Myocardial functional parameters were significantly improved by treatment with telmisartan compared with vehicle-treated rats. Increased myocardial mRNA expressions of inflammatory cytokines [interleukin (IL-6), IL-1β, tumor necrosis factor-α and interferon-γ] were also suppressed by telmisartan treatment compared with vehicle-treated rats. Myocardial protein expressions of NADPH oxidase subunits p47phox, Nox-4, and gp91phox, myocardial levels of 8-hydroxydeoxyguanosine and 4-hydroxy-2-nonenal, and myocardial apoptosis were also significantly decreased by telmisartan treatment compared with vehicle-treated rats. Further, telmisartan significantly decreased endoplasmic reticulum stress markers in experimental autoimmune myocarditis rats. These findings suggest that telmisartan protects against experimental autoimmune myocarditis in rats, at least in part by suppressing inflammatory cytokines and oxidative stress; however, further investigations are needed before clinical use.

Authors+Show Affiliations

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

Language

eng

PubMed ID

21115000

Citation

Sukumaran, Vijayakumar, et al. "Telmisartan Ameliorates Experimental Autoimmune Myocarditis Associated With Inhibition of Inflammation and Oxidative Stress." European Journal of Pharmacology, vol. 652, no. 1-3, 2011, pp. 126-35.
Sukumaran V, Watanabe K, Veeraveedu PT, et al. Telmisartan ameliorates experimental autoimmune myocarditis associated with inhibition of inflammation and oxidative stress. Eur J Pharmacol. 2011;652(1-3):126-35.
Sukumaran, V., Watanabe, K., Veeraveedu, P. T., Ma, M., Gurusamy, N., Rajavel, V., Suzuki, K., Yamaguchi, K., Kodama, M., & Aizawa, Y. (2011). Telmisartan ameliorates experimental autoimmune myocarditis associated with inhibition of inflammation and oxidative stress. European Journal of Pharmacology, 652(1-3), 126-35. https://doi.org/10.1016/j.ejphar.2010.10.081
Sukumaran V, et al. Telmisartan Ameliorates Experimental Autoimmune Myocarditis Associated With Inhibition of Inflammation and Oxidative Stress. Eur J Pharmacol. 2011 Feb 10;652(1-3):126-35. PubMed PMID: 21115000.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Telmisartan ameliorates experimental autoimmune myocarditis associated with inhibition of inflammation and oxidative stress. AU - Sukumaran,Vijayakumar, AU - Watanabe,Kenichi, AU - Veeraveedu,Punniyakoti T, AU - Ma,Meilei, AU - Gurusamy,Narasimman, AU - Rajavel,Varatharajan, AU - Suzuki,Kenji, AU - Yamaguchi,Ken'ichi, AU - Kodama,Makoto, AU - Aizawa,Yoshifusa, Y1 - 2010/11/27/ PY - 2010/05/19/received PY - 2010/10/26/revised PY - 2010/10/31/accepted PY - 2010/12/1/entrez PY - 2010/12/1/pubmed PY - 2011/4/19/medline SP - 126 EP - 35 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 652 IS - 1-3 N2 - Excess cytokine produced by inflammatory stimuli contributes to the progression of myocardial damage in myocarditis. Angiotensin-II has been shown to play a pivotal role in the pathophysiology of various organs, especially the cardiovascular system. Some angiotensin II type 1 receptor antagonists are reported to inhibit proinflammatory cytokine production in vitro and in vivo. We investigated whether telmisartan, an angiotensin II type 1 receptor antagonist protects against experimental autoimmune myocarditis by suppression of inflammatory cytokines and oxidative stress. Experimental autoimmune myocarditis was induced in Lewis rats by immunization with porcine cardiac myosin. The rats were divided into two groups and treated with either telmisartan (10mg/kg/day) or vehicle for 21days. Age-matched normal rats without immunization were also included in this study. Myocardial functional parameters were significantly improved by treatment with telmisartan compared with vehicle-treated rats. Increased myocardial mRNA expressions of inflammatory cytokines [interleukin (IL-6), IL-1β, tumor necrosis factor-α and interferon-γ] were also suppressed by telmisartan treatment compared with vehicle-treated rats. Myocardial protein expressions of NADPH oxidase subunits p47phox, Nox-4, and gp91phox, myocardial levels of 8-hydroxydeoxyguanosine and 4-hydroxy-2-nonenal, and myocardial apoptosis were also significantly decreased by telmisartan treatment compared with vehicle-treated rats. Further, telmisartan significantly decreased endoplasmic reticulum stress markers in experimental autoimmune myocarditis rats. These findings suggest that telmisartan protects against experimental autoimmune myocarditis in rats, at least in part by suppressing inflammatory cytokines and oxidative stress; however, further investigations are needed before clinical use. SN - 1879-0712 UR - https://www.unboundmedicine.com/medline/citation/21115000/Telmisartan_ameliorates_experimental_autoimmune_myocarditis_associated_with_inhibition_of_inflammation_and_oxidative_stress_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(10)01132-5 DB - PRIME DP - Unbound Medicine ER -