Caixia W.,Yantai University |
Qiusheng Z.,Yantai University |
Yishan W.,Shihezi University |
Xiaoyu C.,Key Laboratory of Xinjiang Endemic Phytomedicine Resources
Proceedings 2011 International Conference on Human Health and Biomedical Engineering, HHBE 2011 | Year: 2011
The aim of this study was to evaluate the anti-metastasis effects and the inhibition of the tube-like structure formation of human umbilical vein endothelial cells ECV304 of isoliquiritigenin and glabridin. The cell survival ratio of mice melanoma cells B16F1 was measured by SRB assay, the lethality rate was tested by trypan blue exclusion test. The survival ratio of human umbilical vein endothelial cells ECV304 were measured by SRB and AO/EB assays. The migration of B16F1 cells and ECV304 cells were measured by scratch wound assay. The matrix metalloproteinase-2 (MMP-2) activity in B16F1 cells culture medium was measured by gelatin zymography and ELISA methods. The inhibition on tube-like structure formation of human umbilical vein endothelial cells ECV304 were detected on artificial basilar membrane rebuilt by matrigel. Taken together, our data suggested that isoliquiritigenin and glabridin have strong anti-metastasis activities, in the same concentration, isoliquiritigenin has stronger function. © 2011 IEEE.
Yuan X.,Qingdao University |
Niu H.-T.,Qingdao University |
Wang P.-L.,Key Laboratory of Xinjiang Endemic Phytomedicine Resources |
Lu J.,Qingdao University |
And 5 more authors.
PLoS ONE | Year: 2015
Flavonoids are important components of 'functional foods', with beneficial effects on cardiovascular function. The present study was designed to investigate whether licochalcone D (LD) could be a cardioprotective agent in ischemia/reperfusion (I/R) injury and to shed light on its possible mechanism. Compared with the I/R group, LD treatment enhanced myocardial function (increased LVDP, dp/dtmax,dp/dtmin, HR and CR) and suppressed cardiac injury (decreased LDH, CK and myocardial infarct size). Moreover, LD treatment reversed the I/ R-induced cleavage of caspase-3 and PARP, resulting in a significant decrease in proinflammatory factors and an increase in antioxidant capacity in I/R myocardial tissue. The mechanisms underlying the antiapoptosis, antiinflammation and antioxidant effects were related to the activation of the AKT pathway and to the blockage of the NF-κB/p65 and p38 MAPK pathways in the I/R-injured heart. Additionally, LD treatment markedly activated endothelial nitric oxide synthase (eNOS) and reduced nitric oxide (NO) production. The findings indicated that LD had real cardioprotective potential and provided support for the use of LD in myocardial I/R injury. © 2015 Yuan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Bo Z.,Key Laboratory of Xinjiang Endemic Phytomedicine Resources |
Bo Z.,Shihezi University |
Chen X.,Key Laboratory of Xinjiang Endemic Phytomedicine Resources |
Jing Z.,Key Laboratory of Xinjiang Endemic Phytomedicine Resources |
And 4 more authors.
Bio-Medical Materials and Engineering | Year: 2014
Non-small-cell lung cancer (NSCLC), the most common type of lung cancers, is resistant to initial chemotherapy intrinsically. The expressions of xenobiotic metabolism genes, antioxidants, and drug efflux proteins are increased in NSCLC. In addition, a redox-sensitive transcription factor named Nrf2 regulates the drug resistance via the expression of electrophile, oxidants detoxification enzymes and efflux mechanism. As was detected by real-time PCR, inhibiting Nrf2 expression through the transfection of shRNA plasmids in A549 cells significantly inhibits the expressions of glutathione pathway genes, antioxidants and multidrug resistance proteins. Using biochemical assays and free radical medical experiments in vitro, it was identified that the RNAi-mediated reduction of Nrf2 expression in lung cancer cells induces the generation of reactive oxygen species, decreases the level of reduced glutathione and results in an increase in the A549 cell proliferation inhibition rate. Thus, targeting Nrf2 activity in NSCLC could be a practical way to inhibit tumor growth and eliminate chemoresistance. © 2014 - IOS Press and the authors.
Yuan X.,Shihezi University |
Li. D.,Shihezi University |
Chen H.,Shihezi University |
Sun C.,Shihezi University |
And 4 more authors.
ICBBT 2010 - 2010 International Conference on Bioinformatics and Biomedical Technology | Year: 2010
Previous reports reveal that Isoliquiritigen(ISL), a licorice flavonoid, possesses various antitumour properties, cyclophosphamide, an alkylating agent, has various genotoxic and carcinogenic effects, and to be involved in some secondary neoplasmas. However, it is still used extensively as an antitumour agent and immunosuppressant in the clinic. In order to find out whether isoliquiritigen could enhance antitumour activity, as well as decrease genotoxic effects of cyclophosphamide or not, the antitumour activity and genotoxic effect of oral intake of ISL combined with intraperitoneal injection of cyclophosphamide was investigated. Mice bearing mouse sarcoma S180 cells and cervical cancer U14 cells were respectively used to estimate the antitumour activity in vivo. The clastogenic activity in bone marrow polychromatic erythrocytes was assayed by frequency of micronucleus. The DNA damage in peripheral white blood cells was assayed by single cell gel electrophoresis. The results indicated that oral administration of ISL (5, 10 and 20 mg/kg body weight) alone has no obvious antitumour activity and genotoxic effect in mice, while ISL synergistically enhanced the antitumour activity of cyclophosphamide (40 mg/kg body weight) in a dose-dependent manner. in addition, ISL can decrease the micronucleus formation in polychromatic erythrocytes and DNA strand breaks in white blood cells in a dose-dependent way. Our results suggested that ISL is able to enhance the antitumour activity and decrease the genotoxic effect of cyclophosphamide. © 2010 IEEE.