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Egyptian Journal of Histology
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Volume Volume 48 (2025)
Volume Volume 47 (2024)
Volume Volume 46 (2023)
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Volume Volume 45 (2022)
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Elsayed, H., Mohammed, W., Gebril, S., Ahmed, S. (2023). The Implication of Cardiac Telocytes, Inflammation, and Apoptosis in Carvedilol Protecttive Effect Against Aluminum Chloride Induced Myocardial Toxicity in Male Wistar Rats. Egyptian Journal of Histology, 46(4), 1563-1577. doi: 10.21608/ejh.2022.141753.1696
Hoda M. Elsayed; Walaa I. Mohammed; Sahar M Gebril; Sanaa A. Ahmed. "The Implication of Cardiac Telocytes, Inflammation, and Apoptosis in Carvedilol Protecttive Effect Against Aluminum Chloride Induced Myocardial Toxicity in Male Wistar Rats". Egyptian Journal of Histology, 46, 4, 2023, 1563-1577. doi: 10.21608/ejh.2022.141753.1696
Elsayed, H., Mohammed, W., Gebril, S., Ahmed, S. (2023). 'The Implication of Cardiac Telocytes, Inflammation, and Apoptosis in Carvedilol Protecttive Effect Against Aluminum Chloride Induced Myocardial Toxicity in Male Wistar Rats', Egyptian Journal of Histology, 46(4), pp. 1563-1577. doi: 10.21608/ejh.2022.141753.1696
Elsayed, H., Mohammed, W., Gebril, S., Ahmed, S. The Implication of Cardiac Telocytes, Inflammation, and Apoptosis in Carvedilol Protecttive Effect Against Aluminum Chloride Induced Myocardial Toxicity in Male Wistar Rats. Egyptian Journal of Histology, 2023; 46(4): 1563-1577. doi: 10.21608/ejh.2022.141753.1696

The Implication of Cardiac Telocytes, Inflammation, and Apoptosis in Carvedilol Protecttive Effect Against Aluminum Chloride Induced Myocardial Toxicity in Male Wistar Rats

Article 2, Volume 46, Issue 4, December 2023, Page 1563-1577  XML PDF (2.86 MB)
Document Type: Original Article
DOI: 10.21608/ejh.2022.141753.1696
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Authors
Hoda M. Elsayed email 1; Walaa I. Mohammed2; Sahar M Gebril3; Sanaa A. Ahmed2
1Department of histology,faculty of medicine,sohag university
2Department of clinical pharmacology, faculty of medicine, sohag university
3Department of histology and cell biology,faculty of medicine,Sohag university
Abstract
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.
Keywords
Cardiac toxicity; carvedilol; caspase 3; oxidative stress; telocytes
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