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1.
Trials ; 18(1): 289, 2017 06 21.
Article in English | MEDLINE | ID: mdl-28637494

ABSTRACT

BACKGROUND: Obesity is a public health concern in many countries due to its increasing prevalence. Euiiyin-tang is an herbal medicine formula often used as a clinical treatment for obesity. It acts to eliminate humidity and purify the blood, the causes of obesity identified by the theoretical framework of Korean medicine. The purpose of this study is to evaluate the efficacy and safety of Euiiyin-tang in treating obesity. METHODS/DESIGN: This study is a randomised, double-blinded and placebo-controlled, multicentre trial. It has two parallel arms: the Euiiyin-tang group and the placebo group. A total of 160 obese adult women will be enrolled in the trial. The participants will be randomly divided at a 1:1 ratio at visit 2 (baseline). The participants will be administered Euiiyin-tang or placebo for 12 weeks. The primary endpoint is the change in weight occurring between baseline and post-treatment. The secondary outcomes include average weight reduction, changes in body fat, waist and hip circumferences, body mass index, and lipid profile, and the results of questionnaires such as the Korean version of Obesity-related Quality of Life, the Korean version of Eating Attitudes Test, the Social Readjustment Rating Scale, and the Stress Reaction Inventory. DISCUSSION: The present study will provide research methodologies for evaluating the efficacy and safety of Euiiyin-tang in patients with obesity. In addition, it will provide evidence of correlation between obesity and Sasang constitutional medicine. TRIAL REGISTRATION: ClinicalTrials.gov, NCT01724099 . Registered on 2 November 2012.


Subject(s)
Anti-Obesity Agents/therapeutic use , Drugs, Chinese Herbal/therapeutic use , Obesity/drug therapy , Weight Loss/drug effects , Adiposity/drug effects , Adolescent , Adult , Aged , Anti-Obesity Agents/adverse effects , Body Mass Index , Clinical Protocols , Double-Blind Method , Drugs, Chinese Herbal/adverse effects , Feeding Behavior , Female , Humans , Lipids/blood , Middle Aged , Obesity/blood , Obesity/diagnosis , Obesity/physiopathology , Quality of Life , Republic of Korea , Research Design , Surveys and Questionnaires , Time Factors , Treatment Outcome , Waist-Hip Ratio , Young Adult
2.
Oncol Rep ; 38(2): 715-724, 2017 Aug.
Article in English | MEDLINE | ID: mdl-28656316

ABSTRACT

Drug resistance in chemotherapy is a serious obstacle for the successful treatment of cancer. Drug resistance is caused by various factors, including the overexpression of P­glycoprotein (P­gp, MDR1). The development of new, useful compounds that overcome drug resistance is urgent. Apigenin, a dietary flavonoid, has been reported as an anticancer drug in vivo and in vitro. In the present study, we investigated whether apigenin is able to reverse drug resistance using adriamycin­resistant breast cancer cells (MCF­7/ADR). In our experiments, apigenin significantly decreased cell growth and colony formation in MCF­7/ADR cells and parental MCF­7 cells. This growth inhibition was related to the accumulation of cells in the sub­G0/G1 apoptotic population and an increase in the number of apoptotic cells. Apigenin reduced the mRNA expression of multidrug resistance 1 (MDR1) and multidrug resistance­associated proteins (MRPs) in MCF­7/ADR cells. Apigenin also downregulated the expression of P­gp. Apigenin reversed drug efflux from MCF­7/ADR cells, resulting in rhodamine 123 (Rho123) accumulation. Inhibition of drug resistance by apigenin is related to the suppression of the signal transducer and activator of transcription 3 (STAT3) signaling pathway. Apigenin decreased STAT3 activation (p­STAT3) and its nuclear translocation and inhibited the secretion of VEGF and MMP­9, which are STAT3 target genes. A STAT3 inhibitor, JAK inhibitor I and an HIF­1α inhibitor decreased cell growth in MCF­7 and MCF­7/ADR cells. Taken together, these results demonstrate that apigenin can overcome drug resistance.


Subject(s)
Apigenin/administration & dosage , Breast Neoplasms/drug therapy , Drug Resistance, Neoplasm/drug effects , STAT3 Transcription Factor/genetics , Apoptosis/drug effects , Breast Neoplasms/genetics , Breast Neoplasms/pathology , Cell Proliferation/drug effects , Doxorubicin/adverse effects , Drug Resistance, Neoplasm/genetics , Female , Gene Expression Regulation, Neoplastic/drug effects , Humans , MCF-7 Cells , Matrix Metalloproteinase 9/genetics , Signal Transduction/drug effects , Vascular Endothelial Growth Factor A/genetics
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