Abstract
Methods The study was undertaken on both normoglycemic and alloxan (90 mg/kg) induced diabetic Sprague Dawley rats weighing 150–250 g. At the completion of the treatment phase (30 days for garlic, 250 mg/kg, oral; 10 days for MET, 70 mg/kg, oral), rats were anesthetized and mounted on the modified Langendorff's apparatus. IRI was produced by myocardial no-flow global ischemia. Developed tension (DT) and heart rate (HR) were recorded both before and after ischemia. The perfusate was collected to estimate the leakage of cardiac biomarkers (Creatine Kinase-MB: CK-MB and Lactate dehydrogenase: LDH). Hearts were removed from the setup and utilized to prepare heart tissue homogenate (HTH) and histological slides. The endogenous antioxidants, superoxide dismutase (SOD) and catalase (CAT), in addition to oxidative thiobarbituric acid substances (TBS), were estimated in HTH. Results The hemodynamic parameters, including percentage recovery in HR and DT, were found significantly higher in animals pretreated with garlic and MET in diabetic rats (DR). Both SOD and CAT enzyme activities increased significantly while TBS levels were reduced in the HTH of animals treated with garlic and MET. The cardiac markers CK-MB and LDH levels also increased in HTH with a corresponding decrease in the perfusate. The histopathological changes in the heart and pancreas demonstrated noticeable protection of the tissues due to pretreatment with garlic and MET. Taken together, these findings advocate that reactive oxygen species derived from hyperglycemia execute an important function in myocardial global IRI; the therapy of garlic homogenate was found to be effective in alleviating these toxic effects. Conclusion The combined therapy of MET and garlic provided synergistic cardioprotection, implying that garlic seems to possess promise in lowering toxic parameters by protecting diabetic induced myocardial injury.
Highlights
Diabetes mellitus (DM), a diverse endocrine illness signified by hyperglycemia, is caused by a deficiency in insulin production, insulin activity, or both
Hyperglycemia, which is caused by insulin insufficiency or insulin resistance (IR), produces reactive oxygen species (ROS), which is the primary basis of diabetic heart (DH) injury. e heart is vulnerable to ROS damage owing to its low number of free radical scavengers
Male Sprague Dawley (SD) rats in a weight range of 150–250 g were kept at standard conditions and unlimited access to food and drink. e animals were kept in an animal house under standard conditions, as directed by the Committee for Control and Supervision of Experiments on Animals (CPCSEA). e experimental protocol was approved by the Institutional Ethical Committee (KCP/IAEC27/2119). ese experiments were conducted in isolated tissues from a perfused heart and were backed up by biochemical and histological data
Summary
Diabetes mellitus (DM), a diverse endocrine illness signified by hyperglycemia, is caused by a deficiency in insulin production, insulin activity, or both. Hyperglycemia, which is caused by insulin insufficiency or IR, produces reactive oxygen species (ROS), which is the primary basis of diabetic heart (DH) injury. E hemodynamic parameters, including percentage recovery in HR and DT, were found significantly higher in animals pretreated with garlic and MET in diabetic rats (DR) Both SOD and CAT enzyme activities increased significantly while TBS levels were reduced in the HTH of animals treated with garlic and MET. E histopathological changes in the heart and pancreas demonstrated noticeable protection of the tissues due to pretreatment with garlic and MET Taken together, these findings advocate that reactive oxygen species derived from hyperglycemia execute an important function in myocardial global IRI; the therapy of garlic homogenate was found to be effective in alleviating these toxic effects. Conclusion. e combined therapy of MET and garlic provided synergistic cardioprotection, implying that garlic seems to possess promise in lowering toxic parameters by protecting diabetic induced myocardial injury
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