Background: Garcinol is a polyisoprenylated benzophenone derived from rinds of fruit of Garcinia species namely Garciniaindica (common name â€˜Kokumâ€™) and Garcinia cambogia (common name â€˜Gombogeeâ€™). Garcinol is not stable and has poor bioavailability which can be improved by complexing garcinol with cyclodextrin (cyclodextringarcinol complex). Objective: The objective of the present study was to investigate effect of cyclodextrin-garcinol complex (20 mg/kg/) on pressure overloadinduced cardiotoxicity and cardiac hypertrophy by aortic stenosis in rats. Methods: Male Wistar rats (250-300g) were divided into following four groups such as: control, sham, stenosis and cyclodextrin-garcinol complex. Daily body weights were recorded. Cyclodextrin-garcinol complex (20 mg/kg/day) in distilled water, was administered orally to rats daily for 18 days and then the animals underwent surgery with aortic binding, the treatment was continued up to 4-6 weeks. Haemodynamic changes and electrocardiogram (ECG) were recorded in anaesthetized rats. Results: Pressure overload induced by arotic stenosis in rat resulted in significant myocardial hypertrophy and decreased endogenous antioxidants when compared with the control and sham group animals. Cyclodextrin-garcinol complex (20 mg/kg) showed significant cardioprotective activity by lowering the myocardial hypertrophy, level of lipid peroxidation (MDA content) as well as elevated the level of GSH. The results suggest pre-treatment of cyclodextrin-garcinol complex (20 mg/kg), may offer potential benefits in the management of cardiotoxicity and cardiac hypertrophy. Conclusion: It is concluded that cyclodextrin-garcinol complex (20 mg/kg) protected the haemodynamics of stenosized heart of rats by reduction of lipid peroxidation and preservation of endogenous antioxidants in rat heart.
How to Cite
Kushawaha, S. K., & Bodhankar, S. (2018). Effect of Cyclodextrin Garcinol Complex on Pressure Overload- Induced Cardiotoxicity and Cardiac Hypertrophy by Aortic Stenosis in Rats. Diabesity, 4(3). https://doi.org/10.15562/diabesity.2018.51