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Hu J.,Fujian University of Traditional Chinese Medicine | Hu J.,Fujian Academy of Traditional Chinese Medicine | Zhao J.,Fujian University of Traditional Chinese Medicine | Chen W.,Fujian University of Traditional Chinese Medicine | And 3 more authors.
Pharmaceutical Biology | Year: 2013

Context: Rubus aleaefolius Poir. (Rosaceae) is used as a folk medicine to treat various types of hepatitis with significant effects in Fujian Province of China. The ethyl acetate fraction of R. aleaefolius root ethanol extract proved effective after our testing in vivo animal experiments. Objective: The protective effects of a major constituent, 1β-hydroxyeuscaphic acid isolated from R. aleaefolius was first investigated against carbon tetrachloride (CCl4)-induced injury in liver cells from hepatocytes cell line (BRL-3A). Materials and methods: Treatment of BRL-3A with CCl4 led to generation of free radicals detected after a 2h incubation and produced cell injury demonstrated by increased leakage of alanine aminotransaminase (ALT) and aspartate aminotransaminase (AST) in the media. Exposure to CCl4 caused apoptosis to cells but did not induce lipid peroxidation. Following treatment with 1β-hydroxyeuscaphic acid at doses ranging from 1 to 100g/mL for 24h, cellular morphology, cell growth function (MTT assay), ALT, AST, malondialdehyde (MDA) and superoxide dismutase (SOD) were assessed and evaluated under control and exposed conditions. Results: The IC50 of 1β-hydroxyeuscaphic acid was 15μg/mL. Exposure of injured BRL-3A at 20μg/mL changed abnormal size, cellular shrinkage, and enhanced regulation. ALT, AST, MDA enzyme levels were reduced and SOD activity was increased. Discussion and conclusion: Treatment with 1β-hydroxyeuscaphic acid has significant hepatoprotective activity by lowering the leakage of intracellular enzymes, reducing the oxidation of proteins and decreasing the incidence of apoptosis. These results provide a basis for confirming the traditional uses of R. aleaefolius in treating hepatic diseases. © 2013 Informa Healthcare USA, Inc. All rights reserved: reproduction in whole or part not permitted. Source

Wang X.-F.,Fujian Academy of Traditional Chinese Medicine | Liu X.-J.,Fudan University | Zhou Q.-M.,Shanghai University of Traditional Chinese Medicine | Du J.,Shanghai University of Traditional Chinese Medicine | And 3 more authors.
Evidence-based Complementary and Alternative Medicine | Year: 2013

Cardiomyocytes apoptosis can lead to heart failure. Conventional and alternative drugs, such as Chinese herbal remedies, have been developed to target cardiomyoblast cells apoptosis. In this study, we investigated the effects of ginsenoside Rb1 (Rb1), an active compound, which is isolated from Notoginseng and Ginseng on isoproterenol-(ISO-) induced apoptosis in rat cardiomyocytes and its mechanism in vivo and in vitro. Rb1 reduced the ISO-induced apoptosis in rat cardiomyocytes and H9c2 cells. The effect of Rb1 was significantly suppressed by H89 (inhibitor for PKA), but not by C-1 (inhibitor for PKC). Based on in-cell blot analysis, the ISO-induced PKA and PKC expressions were decreased by Rb1, which was inhibited by H89, but not by C-1. The expressions of caspase-3 and caspase-9 were decreased after treatment with both ISO and Rb1, but with no change for caspase-8. Our results indicated that Rb1 reducing ISO-induced rat cardiomyocytes apoptosis may be involved in PKA and caspase-9 pathways. © 2013 Xiu-feng Wang et al. Source

Sun Y.,Shanghai University of Traditional Chinese Medicine | Wang X.,Shanghai University of Traditional Chinese Medicine | Wang X.,Fujian Academy of Traditional Chinese Medicine | Zhou Q.,Shanghai University of Traditional Chinese Medicine | And 6 more authors.
Oncology Reports | Year: 2015

In breast cancer, metastasis is the main reason for patient mortality. In the present study, we used breast cancer MDA-MB-231 cells and a mouse xenograft model to demonstrate the effect of emodin on the migration, invasion and metastasis of human breast cancer MDA-MB-231 cells and the related mechanisms. In vitro, wound healing and Transwell assays showed that emodin dose-dependently inhibited the migration and invasion of MDA-MB-231 cells. Enzyme-linked immunosorbent assay (ELISA) showed that emodin decreased the secretion of MMP-2 and MMP-9. Western blot analysis showed that emodin downregulated the expression levels of MMP-2, MMP-9, uPA and uPAR as well as p38 inhibitor SB203580 and ERK inhibitor PD980559, even though TIMP-1 and TIMP-2 were not obviously changed in the MDA-MB-231 cells. Furthermore, emodin inhibited the activity of p38 and ERK1/2 in the MDA-MB-231 cells. In vivo, emodin inhibited lung metastasis in mice bearing the breast cancer MDA-MB-231 xenografts with no obvious changes in body weight, liver and kidney functions. These results indicated that emodin inhibited the lung metastasis of human breast cancer in a mouse xenograft model, and inhibited the invasion of MDA-MB-231 cells associated with the downregulation of MMP-2, MMP-9, uPA and uPAR expression as well as decreased activity of p38 and ERK. Source

Wang X.-F.,Shanghai University of Traditional Chinese Medicine | Wang X.-F.,Fujian Academy of Traditional Chinese Medicine | Zhou Q.-M.,Shanghai University of Traditional Chinese Medicine | Lu Y.-Y.,Shanghai University of Traditional Chinese Medicine | And 4 more authors.
Expert Opinion on Therapeutic Targets | Year: 2015

Introduction: Radix Glycyrrhiza has been used in China for thousand years to treat cancer. However, focus on its tumor-suppressing mechanism has been concentrated on its effect on tumor cell growth and apoptosis.Objectives: With the aid of a panel of human breast cancer cell lines, we reveal that glycyrrhetinic acid (GA), a major component of Radix Glycyrrhiza, is actually a significantly more potent agent to suppress invasion than cell survival.Results: GA effectively inhibits breast cancer cell MMP-2/MMP-9 expression; GA-induced reduction in the MMP-2/9 expression is apparently mediated by GA's ability to specifically inhibit the p38 MAPK activity and its downstream AP1 activation. Moreover, we show that GA down regulates the levels of Fra-1 and c-Jun, two main components of AP1 transcription complex in invasive breast cancer cells and that AP1-specific inhibitor abrogates breast cancer cell invasion. These results suggest that GA impairs the p38 MAPK-AP1 signaling axis, leading to the repression of breast cancer cell invasion. Finally, we demonstrate that GA effectively suppresses breast tumor outgrowth and pulmonary metastasis without causing animal weight loss or eliciting liver/kidney toxicity to the recipient animals.Conclusion: This study indicates that GA represents a good candidate compound for the potential development of therapeutic drug. © 2015 Informa UK, Ltd. Source

Wang D.,Fujian Normal University | Wang P.,Fujian Normal University | Jiang J.,Fujian Normal University | Lv Q.,Fujian Normal University | And 2 more authors.
Journal of Pharmacology and Experimental Therapeutics | Year: 2015

Mas oncogene-related G protein-coupled receptor C (MrgC) is unequally expressed in sensory ganglia and has been shown to modulate pathologic pain. This study investigated the mechanism underlying the effect of MrgC receptors on inflammatory pain. Intrathecal administration of the selective MrgC receptor agonist bovine adrenal medulla 8-22 (BAM8-22) (30 nmol) inhibited complete Freund's adjuvant-evoked hyperalgesia. This was associated with the inhibition of protein kinase C-g and phosphorylated extracellular signal-regulated protein kinase in the spinal cord and/or dorsal root ganglia (DRG). The complete Freund's adjuvant injection in the hindpaw induced an increase in Gq, but not Gi and Gs, protein in the spinal dorsal horn. This increase was inhibited by the intrathecal administration of BAM8-22. The exposure of DRG cultures to bradykinin (10 mM) and prostaglandin E2 (1 mM) increased the expression of calcitonin gene-related peptide (CGRP) and neuronal nitric oxide synthase in small- And medium-sized neurons as well as the levels of CGRP, aspartate, and glutamate in the cultured medium. The bradykinin/prostaglandin E2-induced alterations were absent in the presence of BAM8-22 (10 nM). These results suggest that the activation of MrgC receptors can modulate the increase in the expression of CGRP and neuronal nitric oxide synthase as well as the release of CGRP and excitatory amino acids in DRG associated with inflammatory pain. This modulation results in the inhibition of pain hypersensitivity by suppressing the expression of Gq protein and protein kinase C-g and extracellular signal-regulated protein kinase signaling pathways in the spinal cord and/or DRG. The present study suggests that MrgC receptors may be a novel target for relieving inflammatory pain. Copyright © 2015 by The American Society for Pharmacology and Experimental Therapeutics. Source

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