Lisinopril has a cardio-protective effect on experimental acute autoimmune myocarditis in rats

• Published in: Histology and histopathology Vol. 32; no. 4; p. 405
• Main Authors: Atteya, Muhammad, Mohamed, Raeesa A, Ahmed, Aly M, Abdel-Baky, Nayira A, Alfayez, Musaad A, Almalke, Hatim D, El Fouhil, Ahmed F
• Format: Journal Article
• Language: English
• Published: Spain 01.04.2017
• Subjects: Angiotensin-Converting Enzyme Inhibitors - pharmacology; Animals; Autoimmune Diseases - pathology; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Heart - drug effects; Immunohistochemistry; Lisinopril - pharmacology; Male; Myocarditis - pathology; Random Allocation; Rats; Rats, Wistar
• ISSN: 1699-5848
• DOI: 10.14670/HH-11-809

The present study investigated the effect of lisinopril on experimental autoimmune myocarditis (EAM) in rats, a histologically similar model to human acute myocarditis. Twenty four, six week-old male Wistar rats were randomly allocated into 4 groups of 6 rats each. Group I received no treatment. Group II received lisinopril at a dose of 15 mg/kg/day suspended in 1 ml of 2% gum acacia daily, from day 1 to day 21. To induce myocarditis, animals of groups III and IV were injected by 1 mg of porcine cardiac myosin on days 1 and 8. In addition, animals of group IV received lisinopril in gum acacia daily, from day 1 to day 21. All rats were sacrificed on day 21. Serum levels of creatine phosphokinase, troponin-T, tumor necrosis factor-α and interleukin-6 were estimated. Hearts were processed for histopathological, as well as immunohistochemical study for thioredoxin (TRX) immunoreactivity. The wall of hearts from rats of myocarditis-lisinopril group showed mild focal myocarditis and a significant decrease of the mean percentage of pyknotic nuclei in cardiomyocytes, coincident with a significant decrease in serum biomarkers levels and TRX immunoreactivity, compared to myocarditis group. The present study suggested a cardio-protective effect of lisinopril on acute EAM in rats, probably through a mechanism related to its suppressive effect on angiotensin II formation.