Entanglement of AGE-RAGE axis in cardiac pathosis

Abstract Cardiovascular diseases are the major cause of death globally. Acute coronary syndrome is one of numerous cardiovascular illnesses, including advanced glycation end products (AGEs), which play an instrumental part in their development and progression. A substance with multiple pleiotropic characteristics is rosuvastatin. This study examined the cardioprotective effects of rosuvastatin in isoproterenol-induced myocardial injury, as well as the alterations in advanced glycation end products and their roles in cardiac damage. Rosuvastatin (10 mg/kg, orally) was given to male rats daily for 4 weeks, and on the 29th and 30th days, isoproterenol (85 mg/kg, subcutaneously) was administered to cause cardiac damage. Rats were euthanised on the 31st day, and various samples were collected for examination. Administration of isoproterenol increased cardiac mass, levels of cardiac damage markers, lipid oxidation, and collagen content in the heart. Additionally, it reduced the activities of SOD, CAT, GST, GR, and all other antioxidants. Additionally, isoproterenol raises levels of inflammatory markers including TNF-α and IL-6. It has been observed that advanced glycation end products rise along with heart injury. The AGE-RAGE cascade also messes with the injured heart’s echocardiogram. Additionally, histopathological alterations were noticed. According to the study, rosuvastatin has cardioprotective effects on the experimental model, which were supported by an array of physical, biochemical, and histological characteristics. Summary This study examined the cardioprotective effects of rosuvastatin in isoproterenol-induced myocardial injury, as well as the alterations in advanced glycation end products and their roles in cardiac damage. According to the study, rosuvastatin has cardioprotective effects on the experimental model, which were supported by a number of physiological, biochemical, and histological characteristics. By showing how the functional AGE/RAGE axis is inhibited following rosuvastatin medication, this work provides an etiologic theory involving rosuvastatin therapy in heart injury. These findings may also have practical significance since they highlight the intriguing possibility that rosuvastatin-induced modulation of AGE-RAGE signalling may represent a unique therapeutic approach for the prevention and treatment of other cardiovascular diseases.