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Ozek G.,Anadolu University | Demirci F.,Anadolu University | Ozek T.,Anadolu University | Tabanca N.,University of Mississippi | And 5 more authors.
Journal of Chromatography A | Year: 2010

Four different isolation techniques, conventional hydrodistillation (HD), microwave-assisted hydrodistillation (MWHD), microdistillation (MD) and micro-steam distillation-solid-phase microextraction (MSD-SPME), have been used to analyze the volatile constituents from the aerial parts of Salvia rosifolia Sm. by gas chromatography and gas chromatography coupled to mass spectrometry. HD and MWHD techniques produced quantitatively (yield, 0.39% and 0.40%) and qualitatively (aromatic profile) similar essential oils. α-Pinene (15.7-34.8%), 1,8-cineole (16.6-25.1%), β-pinene (6.7-13.5%), β-caryophyllene (1.4-5.0%) and caryophyllene oxide (1.4-4.4%) were identified as major constituents of this Turkish endemic species. Besides, the hydrodistilled oil of S. rosifolia was evaluated for antibacterial, antifungal, anticancer, antioxidant and cytotoxic activities. The hydrodistilled oil of S. rosifolia showed antibacterial activity against Methicillin-resistant Staphylococcus aureus (MRSA) with a MIC value of 125 μg/mL. Other human pathogenic microorganisms (Escherichia coli, Pseudomonas aeruginosa, Enterobacter aerogenes, Salmonella typhimurium, Staphylococcus epidermidis, Candida albicans) were also inhibited within a moderate range (MIC = 125-1000 μg/mL). Antifungal activity of the oil was also observed against the strawberry anthracnose-causing fungal plant pathogens Colletotrichum acutatum, C. fragariae and C. gloeosporioides. No cytotoxicity was observed for S. rosifolia oil up to 25 mg/mL against malignant melanoma, epidermal, ductal and ovary carcinoma. © 2009 Elsevier B.V. Source

Lee H.-J.,Inje University | Kim K.-W.,Research Institute of Pharmaceutical science | Kim K.-W.,Seoul National University of Science and Technology
Biomolecules and Therapeutics | Year: 2012

The developing embryo naturally experiences relatively low oxygen conditions in vivo. Under in vitro hypoxia, mouse embryonic stem cells (mESCs) lose their self-renewal activity and display an early differentiated morphology mediated by the hypoxiainducible factor-1α (HIF-1α). Previously, we demonstrated that histone deacetylase (HDAC) is activated by hypoxia and increases the protein stability and transcriptional activity of HIF-1α in many human cancer cells. Furthermore HDAC1 and 3 mediate the differentiation of mECSs and hematopoietic stem cells. However, the role of HDACs and their inhibitors in hypoxia-induced early differentiation of mESCs remains largely unknown. Here, we examined the effects of several histone deacetylase inhibitors (HDACIs) on the self-renewal properties of mESCs under hypoxia. Inhibition of HDAC under hypoxia effectively decreased the HIF-1α protein levels and substantially improved the expression of the LIF-specific receptor (LIFR) and phosphorylated-STAT3 in mESCs. In particular, valproic acid (VPA), a pan HDACI, showed dramatic changes in HIF-1α protein levels and LIFR protein expression levels compared to other HDACIs, including sodium butyrate (SB), trichostatin A (TSA), and apicidin (AP). Importantly, our RTPCR data and alkaline phosphatase assays indicate that VPA helps to maintain the self-renewal activity of mESCs under hypoxia. Taken together, these results suggest that VPA may block the early differentiation of mESCs under hypoxia via the destabilization of HIF-1α. © 2012 The Korean Society of Applied Pharmacology. Source

Park Y.-J.,Research Institute of Pharmaceutical science | Song B.,Seoul National University of Science and Technology | Kim Y.-S.,Research Institute of Pharmaceutical science | Kim E.-K.,Research Institute of Pharmaceutical science | And 8 more authors.
Cancer Research | Year: 2013

How myeloid-derived suppressor cells (MDSC) emerge in the tumor environment remains unclear. Here, we report that GM-CSF can convert natural killer (NK) cells into MDSCs. When transferred into tumor-bearing mice, adoptively transferred NK cells lost their NK phenotype and were converted into Ly6ChighLy6Ghigh MDSC. This conversion was abolished by exposure to IL-2 either in vitro or in vivo. Notably, we found that of the 4 maturation stages based on CD11b/CD27 expression levels, only the CD11bhighCD27high NK cells could be converted into CD11bGr1MDSCex vivo. Transfer of CD27highNKcells from tumor-bearing mice into tumor-bearing recipients was associated with conversion to MDSC in a manner associated with reduced numbers of CD11bhighCD27high and CD11bhighCD27lowNKcell populations in the recipients. Our results identify a pathway ofMDSCdevelopment from immature NK cells in tumor-bearing hosts, providing new insights into how tumor cells modulate their host immune microenvironment to escape immune surveillance. © 2013 American Association for Cancer Research. Source

Lee W.,Research Institute of Pharmaceutical science | Kim K.-M.,Kyungpook National University | Bae J.-S.,Research Institute of Pharmaceutical science
American Journal of Chinese Medicine | Year: 2015

The ubiquitous nuclear protein, high mobility group box 1 (HMGB1), is released by activated macrophages and human umbilical vein endothelial cells (HUVECs) and functions as a late mediator of experimental sepsis. Aspalathin (Asp) and nothofagin (Not), which have been reported to have anti-oxidant activity, are the two major active dihydrochalcones found in green rooibos. In this study, we investigated the antiseptic effects and underlying mechanisms of Asp and Not against HMGB1-mediated septic responses in HUVECs and mice. The anti-inflammatory activities of Asp and Not were determined by measuring permeability, monocyte adhesion and migration, and activation of proinflammatory proteins in HMGB1-activated HUVECs and mice. According to the results, Asp and Not effectively inhibited lipopolysaccharide (LPS)-induced release of HMGB1, and suppressed HMGB1-mediated septic responses, such as hyperpermeability, adhesion and migration of leukocytes, and expression of cell adhesion molecules. In addition, Asp and Not suppressed the production of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6), the activation of nuclear factor-κB (NF-κB) and extracellular signal-regulated kinases 1 and 2 (ERK1/2) by HMGB1. Collectively, these results indicate that Asp and Not could be potential therapeutic agents for the treatment of various severe vascular inflammatory diseases via the inhibition of the HMGB1 signaling pathway. © 2015 World Scientific Publishing Company & Institute for Advanced Research in Asian Science and Medicine. Source

Won H.Y.,Center for Cell Signaling and Drug Discovery Research | Min H.J.,Center for Cell Signaling and Drug Discovery Research | Lee W.H.,Research Institute of Pharmaceutical science | Kim S.G.,Research Institute of Pharmaceutical science | Hwang E.S.,Center for Cell Signaling and Drug Discovery Research
Biochemical and Biophysical Research Communications | Year: 2010

G12 family have been known to modulate a variety of cellular events such as cell migration, B cell activation and maturation, cytokine production, and cell differentiation. In particular, Gα12 modulates IgG production, thus induces IgG antibody-mediated immune responses. However, it is largely unknown whether Gα12 is required for T cell-mediated immune functions. In this study, we investigated the effects of Gα12 in the activation and differentiation of CD4+ T cells. While PMA plus ionomycin induced equal levels of IL-2 production in WT and Gα12-deficient lymphocytes, TCR-triggered IL-2 production was significantly attenuated in Gα12 KO lymphocytes. In particular, CD4+ T cells and effector Th cells lacking of Gα12 revealed diminished IL-2 production, but not IFNγ production, upon TCR stimulation. In addition, supplement of IL-2 preferentially induced Gα12-deficient CD4+ T cells into Th2 and Th17 cells; however, the expression of specific transcription factors was unchanged in Gα12 KO Th cells. While IL-2 expression was still diminished by the re-stimulation with anti-CD3, PMA plus ionomycin restored IL-2 production in Gα12-deficient Th1 and Th2 cells. These results suggest that Gα12 may be a critical signaling molecule in TCR-induced IL-2 production and also relay a signal to suppress Th2 and Th17 cell differentiation. © 2010 Elsevier Inc. All rights reserved. Source

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