ginsenoside-m1 and Chronic-Disease

Depression is a major social and health problem worldwide. Compound K (CK), an intestinal metabolite of panaxadiol ginsenosides, has been demonstrated to possess significant pharmacological effects on the central nervous system (CNS). Here, we set up this study to investigate the antidepressant effect of CK, and to explore the potential mechanisms underlying this activity. The behavioral despair model and chronic unpredictable mild stress (CUMS) model were established in mice or rats, respectively. Forced swimming test (FST), tail suspension test (TST) and locomotor activity were performed in mice, while the open-field test, food consumption and sucrose preference were assessed in rats. To investigate the underlying mechanism, the levels of endogenous noradrenaline, dopamine (DA), 5-hydroxytryptamine (5-HT) and their metabolites in the prefrontal cortex (PFC) and hippocampus were detected by HPLC coupled with electron detector. The dopamine degradation enzyme (COMT and MAO) expression was measured by western blot. The BDNF and NGF expression were investigated by immunohistochemical staining analysis. The results showed CK (10, 30 mg/kg) intragastric administration for 14 days significantly shorten the immobility time in FST and TST, which could be partially reversed by a D1 receptor antagonist Sch23390. For CUMS rats, CK alleviated the depressant-like behaviors, including decreased food consumption, spontaneous locomotor activity and lower sucrose preference, while WAY-100635, a 5-HT

Topics: Animals; Antidepressive Agents; Chronic Disease; Dopamine; Dose-Response Relationship, Drug; Ginsenosides; Hindlimb Suspension; Hippocampus; Male; Mice; Random Allocation; Serotonin; Stress, Psychological; Swimming

To investigate the protective effects of protopanaxadiol-type ginsenoside (PDG) and its metabolite ginsenoside M1 (G-M1) on carbon tetrachloride (CCl(4))-induced chronic liver injury in ICR mice, we carried out conversion of protopanaxadiol-type ginsenosides to ginsenoside M1 using snailase. The optimum time for the conversion was 24 h at a constant pH of 4.5 and an optimum temperature of 50 °C. The transformation products were identified by high-performance liquid chromatography and electrospray ion-mass spectrometry. Subsequently, most of PDG was decomposed and converted into G-M1 by 24 h post-reaction. During the study on hepatoprotective in a mice model of chronic liver injury, PDG or G-M1 supplement significantly ameliorated the CCl(4)-induced liver lesions, lowered the serum levels of select hepatic enzyme markers (alanine aminotransferase, ALT, and aspartate aminotransferase, AST) and malondialdehyde and increased the activity of superoxide dismutase in liver. Histopathology of the liver tissues showed that PDG and G-M1 attenuated the hepatocellular necrosis and led to reduction of inflammatory cell infiltration. Therefore, the results of this study show that PDG and G-M1 can be proposed to protect the liver against CCl(4)-induced oxidative injury in mice, and the hepatoprotective effect might be attributed to amelioration of oxidative stress.

Topics: Alanine Transaminase; Animals; Antioxidants; Aspartate Aminotransferases; Biotransformation; Body Weight; Carbon Tetrachloride; Chemical and Drug Induced Liver Injury; Chromatography, High Pressure Liquid; Chronic Disease; Ginsenosides; Liver; Male; Malondialdehyde; Mice; Mice, Inbred ICR; Organ Size; Protective Agents; Sapogenins; Snails; Spectrometry, Mass, Electrospray Ionization; Superoxide Dismutase; Tissue Extracts

During the screening program to discover antipsoriatic agents from natural products, ginseng was found to show inhibitory activity in oxazolone-induced mouse ear dermatitis. Therefore, the effects of a main constituent ginsenoside Rb1 isolated from ginseng and its metabolite compound K on oxazolone-induced mouse ear dermatitis were investigated. Compound K at concentrations of 0.02% and 0.05% also potently suppressed mouse ear swelling by 54% and 76% at 16 days, respectively, although ginsenoside Rb1 did not significantly show the inhibitory activity. The compound K also significantly reduced the levels of mRNA of cyclooxygenase (COX)-2, IL-1beta, TNF-alpha, IFN-gamma and IL-4 increased in oxazolone-applied mouse ears. Based on these findings, the compound K may improve contact dermatitis or psoriasis by the regulation of COX-2 produced by macrophage cells and interferon-gamma and IL-4 induced by Th cells.

Topics: Animals; Cell Line; Chronic Disease; Cyclooxygenase 1; Cyclooxygenase 2; Dermatitis, Contact; Dinoprostone; Female; Ginsenosides; Macrophages; Membrane Proteins; Mice; Mice, Inbred ICR; Nitric Oxide; Oxazolone; Prostaglandin-Endoperoxide Synthases; Psoriasis; RNA, Messenger