Inhibitory effects of Hibiscus sabdariffa L extract on low‐density lipoprotein oxidation and anti‐hyperlipidemia in fructose‐fed and cholesterol‐fed rats

Hibiscus sabdariffa L extract (HSE) is an aqueous extract of Hibiscus sabdariffa L flowers that is used as a local soft drink and medical herb in Taiwan. Oxidation of low‐density lipoprotein (LDL) has been shown to increase the incidence of atherosclerosis. In this study, we determined the antioxidative activity of HSE on LDL oxidation by examining relative electrophoretic mobilities (REM) and thiobarbituric acid‐reactive substances (TBARS). The data revealed an inhibitory effect of HSE on Cu²⁺‐mediated REM and TBARS. HSE exhibited a remarkable ability to reduce cholesterol degradation and ApoB fragmentation. Overall, HSE showed a high potency to inhibit the production of oxidized LDL induced by copper and, specifically, to reduce serum triglycerides in high‐fructose diet (HFD) fed rats and serum cholesterol in high‐cholesterol diet (HCD) fed animals. The levels of LDL and the ratio of LDL‐cholesterol (LDL‐C) to HDL‐cholesterol (HDL‐C) were reduced by HSE in both hyperlipidaemia models. Based on these findings, we suggest that HSE may be used to inhibit LDL oxidation and to prevent various types of hyperlipidaemia in HFD‐ or HCD‐fed rats. Copyright © 2004 Society of Chemical Industry     

Consumption of Hibiscus sabdariffa L. aqueous extract and its impact on systemic antioxidant potential in healthy subjects

BACKGROUND: To evaluate health benefits attributed to Hibiscus sabdariffa L. a randomized, open‐label, two‐way crossover study was undertaken to compare the impact of an aqueous H. sabdariffa L. extract (HSE) on the systemic antioxidant potential (AOP; assayed by ferric reducing antioxidant power (FRAP)) with a reference treatment (water) in eight healthy volunteers. The biokinetic variables were the areas under the curve (AUC) of plasma FRAP, ascorbic acid and urate that are above the pre‐dose concentration, and the amounts excreted into urine within 24 h (Ae_0–24) of antioxidants as assayed by FRAP, ascorbic acid, uric acid, malondialdehyde (biomarker for oxidative stress), and hippuric acid (metabolite and potential biomarker for total polyphenol intake). RESULTS: HSE caused significantly higher plasma AUC of FRAP, an increase in Ae_0–24 of FRAP, ascorbic acid and hippuric acid, whereas malondialdehyde excretion was reduced. Furthermore, the main hibiscus anthocyanins as well as one glucuronide conjugate could be quantified in the volunteers' urine (0.02% of the administered dose). CONCLUSION: The aqueous HSE investigated in this study enhanced the systemic AOP and reduced the oxidative stress in humans. Furthermore, the increased urinary hippuric acid excretion after HSE consumption indicates a high biotransformation of the ingested HSE polyphenols, most likely caused by the colonic microbiota. Copyright © 2012 Society of Chemical Industry     

6‐Dehydrogingerdione,an active constituent of dietary ginger,induces cell cycle arrest and apoptosis through reactive oxygen species/c‐Jun N‐terminal kinase pathways in human breast cancer cells

This study is the first to investigate the anticancer effect of 6‐dehydrogingerdione (DGE), an active constituent of dietary ginger, in human breast cancer MDA‐MB‐231 and MCF‐7 cells. DGE exhibited effective cell growth inhibition by inducing cancer cells to undergo G2/M phase arrest and apoptosis. Blockade of cell cycle was associated with increased levels of p21, and reduced amounts of cyclin B1, cyclin A, Cdc2 and Cdc25C. DGE also enhanced the levels of inactivated phosphorylated Cdc2 and Cdc25C. DGE triggered the mitochondrial apoptotic pathway indicated by a change in Bax/Bcl‐2 ratios, resulting in caspase‐9 activation. We also found the generation of reactive oxygen species is a critical mediator in DGE‐induced cell growth inhibition. DGE clearly increased the activation of apoptosis signal‐regulating kinase 1 and c‐Jun N‐terminal kinase (JNK), but not extracellular signal‐regulated kinase 1/2 (ERK1/2) and p38. In addition, antioxidants vitamin C and catalase significantly decreased DGE‐mediated JNK activation and apoptosis. Moreover, blocking JNK by specific inhibitors suppressed DGE‐triggered mitochondrial apoptotic pathway. Taken together, these findings suggest that a critical role for reactive oxygen species and JNK in DGE‐mediated apoptosis of human breast cancer.     

Effect of flavonol glycoside in mulberry (Morus alba L.) leaf on glucose metabolism and oxidative stress in liver in diet‐induced obese mice

BACKGROUND: Mulberry therapies on type 2 diabetic patients or streptozotocin‐induced diabetic rats have been reported to improve fasting blood glucose levels. We investigated the effects of dietary consumption of mulberry‐leaf powder and purified quercetin 3‐(6‐malonylglucoside), the quantitatively major flavonol glycoside in mulberry leaves, on glucose and lipid metabolism in high‐fat diet‐induced obese mice. Male C57BL/6J mice aged 8 weeks were assigned to three groups (control, mulberry leaf powder (MLP), and quercetin 3‐(6‐malonylglucoside) (Q3MG)) and treated with their respective diets for 8 weeks. RESULTS: We found that dietary supplementation of 10 g MLP kg^?1 or 1 g Q3MG kg^?1 in high‐fat diet effectively suppressed blood glucose levels. We also noted increased expression of glycolysis‐related genes and suppression of thiobarbituric acid reactive substances concentrations in the liver of Q3MG group compared to control mice. CONCLUSION: Dietary consumption of Q3MG, the quantitatively major flavonol glycoside in mulberry leaves, improved hyperglycemia in obese mice and reduced oxidative stress in the liver. Copyright © 2010 Society of Chemical Industry