Caesalpinia sappan L. ameliorates hypercholesterolemia in C57BL/6 mice and suppresses inflammatory responses in human umbilical vein endothelial cells (HUVECs) by antioxidant mechanism.
कीवर्ड
सार
Oxidative stress and inflammatory mediators were measured in the plasma and livers of C57BL/6 mice fed a high-cholesterol diet for 14 weeks and in cultured human umbilical vein endothelial cells (HUVECs). Some of the mice fed with the atherogenic diet received drinking water supplemented with 0.01 g of a 70% ethanol extract of Caesalpinia sappan L. (CSLE) per 20 g of body weight. Numerous parameters were determined: concentrations of total, high-, and low-density cholesterol; atherogenic index; plasma trolox equivalent antioxidant capacity (TEAC); levels of hepatic thiobarbituric acid reactive substances (TBARS) and protein carbonyls; and the activities of hepatic antioxidant enzymes, including Cu·Zn-SOD, Mn-SOD, glutathione peroxidase, glutathione reductase, and catalase. HUVECs were stimulated with tumor necrosis factor α (TNFα) and the expression of intracellular reactive oxygen species (ROS), lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), adhesion molecules, inhibitory κBα (IκBα), and nuclear factor κB (NFκB) were measured. Compared to mice fed a hypercholesterolemic diet alone, mice fed a hypercholesterolemic diet supplemented with CSLE exhibited decreased total plasma cholesterol and increased high-density lipoprotein cholesterol, and thus a lower atherogenic index. Furthermore, plasma TEAC and levels of hepatic TBARS and protein carbonyls were significantly decreased in CSLE-supplemented mice (P < 0.05), whereas all hepatic antioxidative indicators were significantly elevated (P < 0.05). In HUVECs stimulated with TNFα, CSLE significantly decreased the expression of intracellular ROS, LOX-1, and adhesion molecules; the degradation of IκBα; and the nuclear translocation of NFκB; in contrast, CSLE induced the expression of Nrf2 and HO-1 (P < 0.05 for all results).