stilbenes and naringin

To develop a qualitative and quantitative determination of multiple components for quality control of Hugu Capsule, a composite prescription in TCM.. HPLC analysis was performed on a Kromasil C18 column (5.0 microm, 250 mm x 4.6 mm) by gradient elution with methanol-acetonitrile-1% glacial acetic acid as the mobile phase at a flow-rate of 0.8 mL/min,the detection wavelengths were set at 270, 283, 320 and 325 nm at the temperature of 30 degrees C.. Five components: chlorogenic acid, tetrahydroxy stilbene glucoside, ferulaic acid, naringin and icariin were simultaneously analyzed in this study. The calibration curves were exhibited linear regressions of at least r > 0.9992. The injection precision,the intra-day precisions and the analysis repeatability were evaluated with the RSD values were all less than 5%. The mean recoveries of the five components were ranged from 97.4% to 99.4%, and RSD values all were less than 1.72%.. This method is found to be convenient, fast, accurate, and is applicable to analyze the multi-constituents in Hugu Capsule.

Topics: Capsules; Chlorogenic Acid; Chromatography, High Pressure Liquid; Coumaric Acids; Drug Combinations; Drugs, Chinese Herbal; Flavanones; Flavonoids; Glucosides; Quality Control; Reproducibility of Results; Stilbenes

Recently, several flavonoids have been shown to have cardioprotective, cancer preventive, or anti-inflammatory properties. However, the specific mechanisms underlying their protective effects remain unclear. We aimed to investigate the different effects of three representative flavonoids-hesperidin, naringin, and resveratrol-on intracellular adhesion molecule-1 (ICAM-1) induction in human umbilical vein endothelial cells (HUVECs) by using high-glucose (HG) concentrations and the possible underlying molecular mechanisms. In HG-induced HUVEC cultures, the effects of three different flavonoids on ICAM-1 production and p38 phosphorylation were examined in the presence or absence of inhibitors targeting the mitogen-activated protein kinase (MAPK) signal transduction pathway. HG stimulation of HUVECs increased the levels of the adhesion molecules ICAM-1 and endothelial selectin (E-selectin). Pretreatment with all the three flavonoids drastically inhibited ICAM-1 expression in a time-dependent manner, but did not alter VCAM-1 and E-selectin expressions. Moreover, we investigated the effects of flavonoids on the MAPK signal transduction pathway, because MAPK families are associated with vascular inflammation under stress. These flavonoids did not block HG-induced phosphorylation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK), but completely inhibited the HG-induced phosphorylation of p38 MAPK. SB202190, an inhibitor of p38 MAPK, also inhibited the HG-induced enrichment of ICAM-1. This study demonstrated that hesperidin, naringin, and resveratrol reduced the HG-induced ICAM-1 expression via the p38 MAPK signaling pathway, contributing to the inhibition of monocyte adhesion to endothelial cells.

Topics: Anthracenes; Butadienes; Cells, Cultured; Endothelium, Vascular; Enzyme Inhibitors; Flavanones; Glucose; Hesperidin; Humans; Hyperglycemia; Imidazoles; Intercellular Adhesion Molecule-1; Nitriles; p38 Mitogen-Activated Protein Kinases; Pyridines; Resveratrol; Stilbenes; Up-Regulation; Veins

Sirt1, a deacetylase involved in regulating energy metabolism in response to calorie restriction, is up regulated after chronic ethanol feeding using the intragastric feeding model of alcohol liver disease. PGC1 alpha is also up regulated in response to ethanol. These changes are consistent with activation of the Sirt1/PGC1 alpha pathway of metabolism and aging, involved in alcohol liver disease including steatosis, necrosis and fibrosis of the liver. To test this hypothesis, male rats fed ethanol intragastrically for 1 month were compared with rats fed ethanol plus resveratrol or naringin. Liver histology showed macrovesicular steatosis caused by ethanol and this change was unchanged by resveratrol or naringin treatment. Necrosis occurred with ethanol alone but was accentuated by resveratrol treatment, as was fibrosis. The expression of Sirt1 and PGC1 alpha was increased by ethanol but not when naringin or resveratrol was fed with ethanol. Sirt3 was also up regulated by ethanol but not when resveratrol was fed with ethanol. These results support the concept that ethanol induces the Sirt1/PGC1 alpha pathway of gene regulation and both naringin and resveratrol prevent the activation of this pathway by ethanol. However, resveratrol did not reduce the liver pathology caused by chronic ethanol feeding.

Topics: Animals; Energy Metabolism; Ethanol; Feeding Behavior; Flavanones; Liver; Male; PPAR gamma; Rats; Rats, Wistar; Resveratrol; Sirtuin 1; Sirtuins; Stilbenes; Up-Regulation