Citation
Amom, Zulkhairi and Bahari, Hasnah and Md Shah, Zamree and Mohd Arshad, Mohd Shahidan and Ibrahim, Nursakinah and Othman, Fauziah and Ismail, Maznah and Baharuldin, Mohamad Taufik Hidayat and Mohd Moklas, Mohamad Aris and Abdul Kadir, Khairul Kamilah
(2009)
Potential of Tinospora crispa as a Hypocholesterolemic agent in rabbits.
Malaysian Journal of Medicine and Health Sciences, 5 (2).
pp. 1-10.
ISSN 1675-8544
Abstract
Introduction: Hypercholesterolemia is the major cause of cardiovascular disturbances. The influence of Tinospora crispa on atherosclerotic plaque formation in rabbits fed with high cholesterol diet was investigated. Methods: Thirty male New Zealand White rabbits were divided into 6 groups. The negative control (NC) and positive control (PC) groups were used as a negative and positive (0.5% cholesterol) control. The simvastatin control (SC) group was given a high cholesterol diet (HCD) with 5mg/kg simvastatin. Treatment groups T150 and T450 were given HCD with supplementation of 150,300 and 450mg/kg of T.crispa extract respectively for 10 weeks. Blood was collected from ear vein for plasma analysis while the aortas were excised and examined microscopically. Results: Comparison within groups showed that PC, T300 and T450 had a significant increase (p<0.05) in total cholesterol level throughout the study. The groups supplemented with T.crispa (T150, T300 and T450) were significantly higher (p<0.05) in high density lipoprotein (HDL) level by 10.7-fold, significantly higher (p<0.05) in total antioxidant activity and had a significantly lower (p<0.05) LDL level compared to PC at week 10. At week 10, T450 had significantly highest (p<0.05) glutathione peroxidase and superoxide dismutase levels compared to PC. No foam cell formation was visible in the aorta of rabbits,in groups NC,SC and T450. However , there was visible foam cell formation in the aorta of groups PC, T150 and T300. Conclusion: This study suggest that supplementation of 450mg/kg of T.crispa extract would be able to reduce or retard the progression of atherosclerotic plaque development induced by dietary cholesterol.
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