Gallic acid protects against isoproterenol-induced cardiotoxicity in rats

Author:

Shackebaei Dareuosh12,Hesari Mahvash1,Ramezani-Aliakbari Soudabeh13,Hoseinkhani Zohreh1,Ramezani-Aliakbari Fatemeh14ORCID

Affiliation:

1. Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran

2. Cardiovascular Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran

3. Medical School, Kermanshah University of Medical Sciences, Kermanshah, Iran

4. Department of Physiology, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran

Abstract

Background Gallic acid (GA) is a polyphenolic agent with interesting pharmacological impacts on the cardiovascular system. Objective The present study purposed to study the protective effects of GA at 25 and 50 mg/kg against isoproterenol (ISO)-induced cardiac damage in ischemia/reperfusion (I/R) in rats. Methods Male Wistar rats were randomly assigned into six groups: Control, Control treated with GA at 25 mg/kg (GA25), Control treated with GA at 50 mg/kg (GA50), Hypertrophic rats induced by ISO (ISO), Hypertrophic rats treated with GA at 25 mg/kg (ISO+GA25), and Hypertrophic rats treated with GA at 50 mg/kg (ISO+GA50). Heart isolation was performed to induce a cardiac I/R injury model. Cardiac hemodynamic parameters were recorded. Serum Lactate Dehydrogenase (LDH) and Creatine Kinase-MB (CK-MB) and cardiac Superoxide dismutases (SOD) levels were evaluated. The gene expression of Sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) was assessed. Results We found that GA at 50 mg/kg was significantly increased cardiac function at post I/R period in ISO-induced hypertrophic hearts. Moreover, it suppressed cardiac hypertrophy, the serum LDH and CK-MB levels in ISO injected rats. Administration of GA at 50 mg/kg was significantly increased SOD level and SERCA2a gene expression in the hypertrophic hearts. Conclusion GA at 50 mg/kg could improve cardiac performance possibly by increasing antioxidant defense enzymes, reducing cell damage, and enhancing SERCA2a gene expression in hypertrophic heart induced by ISO in I/R injury conditions.

Funder

Medical Biology Research Center, Kermanshah University of Medical Sciences

Publisher

SAGE Publications

Subject

Health, Toxicology and Mutagenesis,Toxicology,General Medicine

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