Effect of gallic acid and Terminalia chebulaon hepatic oxidative stress markers of high fat diet induced hyperlipidemicmice
Keywords:Terminalia chebula, hyperlipidemic activity, oxidative stress markers
Introduction and Aim:Hyperlipidemia is caused due to lipid abnormalities leading to lipid peroxidation which causes extensive damage to hepatic tissues. The aim of the study is to induce hyperlipidemia in mice using high fat diet (HFD) and to estimate the effect of gallic acid and Terminalia chebula in reducing hepatic oxidative stress caused by hyperlipidemia.
Materials and Methods:36 C57BL/6J Male18 ±3 g was divided into four groups; group I(6): received normal diet for 16 weeks, group II(10). High fat diet (HFD) + 0.5% CMC , group III (10)received HFD + gallic acid (50mg/Kg/b.wt) and group IV(10) HFD + T. chebula(250mg/kg/ b.wt)only normal diet for 15 weeks. Tissue samples from liver were taken for determination of reduced glutathione (GSH) levels catalase (CAT), super oxide dismutase (SOD) and Lipid peroxidase(LPO).
Results:The data revealed that feeding the HFD diet significantly raised final body weight and caused hyperlipidemia, which elevated oxidative stress markers.The treatment given to mice HFD + T. chebula (250mg/kg) group IV showed significant increase in antioxidant enzymesand reduced acid reactive substances in blood GSH (47 %p<0.001), CAT (80 % p<0.001),SOD (55 % p<0.001)&LPO (48 % p<0.001) than mice of group III HFD + gallic acid (50mg/Kg/b.wt) GSH (32 % p<0.001), CAT (40 % p<0.001),SOD (31 % p<0.001)&LPO (38 % p<0.01).
Conclusion:High fat diet-induced hyperlipidemia is coupled with increased hepatic oxidative stress, which is characterized by a decrease in antioxidant enzymes activityand increased lipid peroxidationis being more effectively treated by T. chebula powder than gallic acid (pure compound).
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