Atherosclerosis is a pathology related to oxidative stress and inflammation. Prevention of atherosclerosis can be achieved by blocking the oxidation and inflammation process that occurs on the endothelial cells. Tinospora cispa, a climber that is commonly found in primary rainforest is widely distributed in Malaysia, Indonesia, Thailand and Vietnam. T. cispa which has been claimed to exert various health promoting effects has been reported to possess anti-diabetic, anti-malarial and antiinflammatory properties. This study sought to investigate the effect of T. crispa extracts in preventing oxidative stress and inflammation induced by hydrogen peroxide (H 2 O 2) and tumor necrosis factor (TNF)-α, respectively. Human umbilical vein endothelial cells (HUVECs) were cultured on 6-wells plate before treated by TCAE and TCME at various concentrations (100, 200, 400 and 600 µg/ml). After 30 min of incubation, H 2 O 2 or TNF-α (10 ng/ml) was administered on HUVECs. HUVECs were harvested after 24 h and tested for CAT, SOD, GPx, MDA, ICAM-1, VCAM-1 and NO using various kit. The result showed that TCAE and TCME showed modulatory effect on H 2 O 2-induced CAT, SOD and GPx activity. Concomitantly, MDA level was reduced by pretreatment of TCAE and TCME for 24 h. In addition, TCAE and TCME showed an inhibitory effect on TNF-α induced secretion of ICAM-1, VCAM-1 signaling molecule while NO secretion was increased. Therefore, these results showed a protective effect of T. crispa extracts on the H 2 O 2-induced oxidative stress and TNF-α-induced inflammation.
In this study, the ability of Tinospora crispa aqueous extract (TCAE) to regulate cholesterol metabolism in human hepatoma cancer cell line (Hep G2) was determined. Cytotoxic study was performed by exposing hepatoma cell (Hep G2) towards TCAE with concentration ranging from 0.002 to 20 mg/ml for 24 h at 37°C and with 5% CO 2 atmosphere. Result revealed that TCAE was not toxic to the cell. The ability of TCAE to reduce cholesterol in cell culture experiment was carried out by pre-treating Hep G2 with selected concentrations of TCAE (10, 5, 2.5, 1.25 and 0.625 mg/ml) in 6-well plate before the cell was exposed to low density lipoprotein (LDL). The concentration of apolipoprotein A1 (Apo A1), lecithin-cholesterol acyltransferase (LCAT), low density lipoprotein receptor (LDLR), scavenger receptor B1 (SRB1) and hepatic Lipase (HL) which involve in reverse cholesterol transport (RCT) pathway were determined from the 6-well plate medium. The direct pathway of cholesterol synthesis was performed according to the instruction provided in HMG-CoA Reductase Assay Kit manuals. The results showed that TCAE significantly increase (p<0.05) the concentration of Apo A1, LCAT, LDLR, SRB-1 and HL. The efficacy of these activities is appreciably good when compared with standard drug simvastatin. However, TCAE showed moderate effect in controlling mevalonate pathway. These findings suggested that TCAE has the potential to reduce cholesterol metabolism in Hep G2 cancer cell lines and the pathway of TCAE action possibly more on RCT.
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