Jayaraman Rajangam1, Navaneetha Krishnan1, Narahari N Palei2,3, Shvetank Bhatt4, Manas Kumar Das5, Saumya Das6, Krishnapillai Mathusoothanan7. 1. Sree Vidyanikethan College of Pharmacy, Department of Pharmacology, Andhra Pradesh, India 2. Sree Vidyanikethan College of Pharmacy, Department of Pharmaceutics, Andhra Pradesh, India 3. The Neotia University School of Pharmacy, Department of Pharmaceutics, West Bengal, India 4. Amity University Amity Institute of Pharmacy, Department of Pharmacology, Madhya Pradesh, India 5. Orlean College of Pharmacy, Department of Pharmacology, Uttar Pradesh, India 6. NIET College of Pharmacy, Department of Pharmacology, Uttar Pradesh, India 7. Grace College of Pharmacy, Department of Pharmaceutics, Kerala, India
Abstract
Objectives: The study aimed to explore the in vivo protective potential of rosuvastatin (ROSS), an oral antihyperlipidemic drug against doxorubicin (DOXO) induced cardio toxicity in rats. Materials and Methods: Cardiac toxicity was induced by DOXO injection (10 mg/kg, i.p.), once on the 20th day of the experiment. Except for the control rats, all were received DOXO and the study was continued for up to 21 days. The influence of ROSS on acute treatment was analyzed by quantification of cardiac marker enzymes such as creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) and liver marker enzymes like aspartate aminotransferase (AST), alanine aminotransferase (ALT) along with the measurement of in vivo antioxidants like superoxide dismutase and catalase. To observe histological changes of myocardial tissue hematoxylin and eosin staining were used. Results: Acute administration of DOXO resulted in a marked rise of cardiac marker enzymes that confirms the myocardial damage compared to control animals whereas administration of ROSS (10 mg/kg, p.o.) resulted in the significant reduction of CK-MB, LDH levels (p<0.05) and AST, ALT levels to a remarkable extent. Moreover, ROSS administration significantly increased the activities of various in vivo antioxidant levels. Conclusion: From the results, the acute administration of ROSS showed significant cardioprotective property, which was evidenced by a significant reduction of cardiac and liver marker enzymes along with significant improvement of in vivo antioxidant activities. Furthermore the results were supported with histopathological observations. Hence, it can be concluded that cardioprotective potential of ROSS may be through attenuation of oxidative stress by modulating oxidative damage in rats.
Objectives: The study aimed to explore the in vivo protective potential of rosuvastatin (ROSS), an oral antihyperlipidemic drug against doxorubicin (DOXO) induced cardio toxicity in rats. Materials and Methods: Cardiac toxicity was induced by DOXO injection (10 mg/kg, i.p.), once on the 20th day of the experiment. Except for the control rats, all were received DOXO and the study was continued for up to 21 days. The influence of ROSS on acute treatment was analyzed by quantification of cardiac marker enzymes such as creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) and liver marker enzymes like aspartate aminotransferase (AST), alanine aminotransferase (ALT) along with the measurement of in vivo antioxidants like superoxide dismutase and catalase. To observe histological changes of myocardial tissue hematoxylin and eosin staining were used. Results: Acute administration of DOXO resulted in a marked rise of cardiac marker enzymes that confirms the myocardial damage compared to control animals whereas administration of ROSS (10 mg/kg, p.o.) resulted in the significant reduction of CK-MB, LDH levels (p<0.05) and AST, ALT levels to a remarkable extent. Moreover, ROSS administration significantly increased the activities of various in vivo antioxidant levels. Conclusion: From the results, the acute administration of ROSS showed significant cardioprotective property, which was evidenced by a significant reduction of cardiac and liver marker enzymes along with significant improvement of in vivo antioxidant activities. Furthermore the results were supported with histopathological observations. Hence, it can be concluded that cardioprotective potential of ROSS may be through attenuation of oxidative stress by modulating oxidative damage in rats.
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