Introduction: Aluminum is a widespread metal in the environment and linked to several diseases, including cardiovascular disease. Regenerative cardiac telocytes can potentially alleviate numerous heart diseases.
Aim of the Work: This study investigated the potential protective effect carvedilol on aluminum trichloride (AlCl3)-induced cardiac toxicity by examining its antioxidative, anti-inflammatory, anti-apoptotic and its impact on cardiac telocytes.
Materials and Methods: Thirty adult male Wistar rats were randomly divided into three (10-rats) groups. Control group: saline. AlCl3 group: after two weeks of saline, (70 mg/kg/day) AlCl3 for four weeks. The Carvedilol+ AlCl3 group: (1 mg/kg day) carvedilol for two weeks followed by AlCl3 for four weeks. All drugs were received as a single dose daily I.P. At the end of the experiment, blood biochemical antioxidants, inflammatory and aluminum level were assessed. Additionally cardiac tissue histology, immunohistochemistry (active caspase 3 and CD117 markers) and histomorphometry were performed.
Results: Administration of AlCl3 significantly increase in cardiac malonaldehyde, nitric oxide, and tumor necrosis factor-alpha levels as well as both serum and cardiac aluminum levels. Heart and body weights and cardiac catalase levels were significantly decreased. Histologically AlCl3 induced degenerative and apoptotic changes in cardiac myocytes with a significant increase in apoptotic cells number and collagen fibers area percentage., However, myocardial telocytes is significantly decreased. Carvedilol administration ameliorated these abnormal biochemical, histological and immunohistochemical parameters.
Conclusion: Carvedilol prophylactic administration protected against ALCL3 induced cardiotoxicity via downregulating cardiomyocyte apoptosis and fibrosis due to its antioxidant, anti-inflammatory, and anti-apoptotic effects and increased cardiac telocytes number and its regenerative capacity.