Rongxia Liu
University of Vienna
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Publication
Featured researches published by Rongxia Liu.
British Journal of Pharmacology | 2014
Nanang Fakhrudin; Birgit Waltenberger; M Cabaravdic; Atanas G. Atanasov; Clemens Malainer; Daniel Schachner; Elke H. Heiss; Rongxia Liu; Stefan M. Noha; Anna M. Grzywacz; Judit Mihaly-Bison; E M Awad; Daniela Schuster; Johannes M. Breuss; Judith M. Rollinger; Valery N. Bochkov; Hermann Stuppner; Verena M. Dirsch
The transcription factor NF‐κB orchestrates many pro‐inflammatory signals and its inhibition is considered a promising strategy to combat inflammation. Here we report the characterization of the natural product plumericin as a highly potent inhibitor of the NF‐κB pathway with a novel chemical scaffold, which was isolated via a bioactivity‐guided approach, from extracts of Himatanthus sucuuba, an Amazonian plant traditionally used to treat inflammation‐related disorders.
Scientific Reports | 2016
Elke H. Heiss; Rongxia Liu; Birgit Waltenberger; Shafaat Y. Khan; Daniel Schachner; Paul Kollmann; Kristin Zimmermann; Muris Cabaravdic; Pavel Uhrin; Hermann Stuppner; Johannes M. Breuss; Atanas G. Atanasov; Verena M. Dirsch
The etiology of atherosclerosis and restenosis involves aberrant inflammation and proliferation, rendering compounds with both anti-inflammatory and anti-mitogenic properties as promising candidates for combatting vascular diseases. A recent study identified the iridoid plumericin as a new scaffold inhibitor of the pro-inflammatory NF-κB pathway in endothelial cells. We here examined the impact of plumericin on the proliferation of primary vascular smooth muscle cells (VSMC). Plumericin inhibited serum-stimulated proliferation of rat VSMC. It arrested VSMC in the G1/G0-phase of the cell cycle accompanied by abrogated cyclin D1 expression and hindered Ser 807/811-phosphorylation of retinoblastoma protein. Transient depletion of glutathione by the electrophilic plumericin led to S-glutathionylation as well as hampered Tyr705-phosphorylation and activation of the transcription factor signal transducer and activator of transcription 3 (Stat3). Exogenous addition of glutathione markedly prevented this inhibitory effect of plumericin on Stat3. It also overcame downregulation of cyclin D1 expression and the reduction of biomass increase upon serum exposure. This study revealed an anti-proliferative property of plumericin towards VSMC which depends on plumericin’s thiol reactivity and S-glutathionylation of Stat3. Hence, plumericin, by targeting at least two culprits of vascular dysfunction –inflammation and smooth muscle cell proliferation -might become a promising electrophilic lead compound for vascular disease therapy.
Molecular Nutrition & Food Research | 2015
Rongxia Liu; Elke H. Heiss; Nadine Sider; Andreas Schinkovitz; Barbara Gröblacher; De-An Guo; Rudolf Bauer; Verena M. Dirsch; Atanas G. Atanasov
Scope Vascular smooth muscle cell (VSMC) proliferation is involved in the pathogenesis of cardiovascular disease, making the identification of new counteracting agents and their mechanisms of action relevant. Ginger and its constituents have been reported to improve cardiovascular health, but no studies exist addressing a potential interference with VSMC proliferation. Methods and results The dichloromethane extract of ginger inhibited VSMC proliferation when monitored by resazurin metabolic conversion (IC50 = 2.5 μg/mL). The examination of major constituents from ginger yielded [6]-shogaol as the most active compound (IC50 = 2.7 μM). In the tested concentration range [6]-shogaol did not exhibit cytotoxicity toward VSMC and did not interfere with endothelial cell proliferation. [6]-shogaol inhibited DNA synthesis and induced accumulation of the VSMC in the G0/G1 cell-cycle phase accompanied with activation of the nuclear factor-erythroid 2-related factor 2 (Nrf2)/HO-1 pathway. Since [6]-shogaol lost its antiproliferative activity in the presence of the heme oxygenase-1 (HO-1) inhibitor tin protoporphyrin IX, HO-1 induction appears to contribute to the antiproliferative effect. Conclusion This study demonstrates for the first time inhibitory potential of ginger constituents on VSMC proliferation. The presented data suggest that [6]-shogaol exerts its antiproliferative effect through accumulation of cells in the G0/G1 cell-cycle phase associated with activation of the Nrf2/HO-1 pathway.
Planta Medica | 2015
Christina E. Mair; Rongxia Liu; Atanas G. Atanasov; Wimmer L; Nemetz-Fiedler D; Sider N; Elke H. Heiss; Mihovilovic; Verena M. Dirsch; Judith M. Rollinger
Successful vascular healing after percutaneous coronary interventions is related to the inhibition of abnormal vascular smooth muscle cell proliferation and efficient re-endothelialization. In the search for vascular smooth muscle cell anti-proliferative agents from natural sources we identified piperine (1), the main pungent constituent of the fruits from Piper nigrum (black pepper). Piperine inhibited vascular smooth muscle cell proliferation with an IC50 of 21.6 µM, as quantified by a resazurin conversion assay. Investigations of ten piperamides isolated from black pepper fruits and 15 synthesized piperine derivatives resulted in the identification of three potent vascular smooth muscle cell proliferation inhibitors: the natural alkaloid pipertipine (4), and the two synthetic derivatives (2E,4E)-N,N-dibutyl-5-(3,5-dimethoxyphenyl)penta-2,4-dienamide (14) and (E)-N,N-dibutyl-3-(naphtho[2,3-d][1,3]dioxol-5-yl)acrylamide (20). They showed IC50 values of 3.38, 6.00, and 7.85 µM, respectively. Furthermore, the synthetic compound (2E,4E)-5-(4-fluorophenyl)-1-(piperidin-1-yl)penta-2,4-dien-1-one (12) was found to be cell type selective, by inhibiting vascular smooth muscle cell proliferation with an IC50 of 11.8 µM without influencing the growth of human endothelial cells.
Molecules | 2015
Birgit Waltenberger; Rongxia Liu; Atanas G. Atanasov; Stefan Schwaiger; Elke H. Heiss; Verena M. Dirsch; Hermann Stuppner
Aberrant proliferation of vascular smooth muscle cells (VSMC) plays a major role in restenosis, the pathological renarrowing of the blood vessel lumen after surgical treatment of stenosis. Since available anti-proliferative pharmaceuticals produce unfavorable side effects, there is high demand for the identification of novel VSMC proliferation inhibitors. A natural product screening approach using a resazurin conversion assay enabled the identification of gentisin (1) from Gentiana lutea as a novel inhibitor of VSMC proliferation with an IC50 value of 7.84 µM. Aiming to identify further anti-proliferative compounds, 13 additional nonprenylated xanthones, isolated from different plant species, were also tested. While some compounds showed no or moderate activity at 30 µM, 1-hydroxy-2,3,4,5-tetramethoxyxanthone (4), swerchirin (6), and methylswertianin (7) showed IC50 values between 10.2 and 12.5 µM. The anti-proliferative effect of 1, 4, 6, and 7 was confirmed by the quantification of DNA synthesis (BrdU incorporation) in VSMC. Cell death quantification (determined by LDH release in the culture medium) revealed that the compounds are not cytotoxic in the investigated concentration range. In conclusion, nonprenylated xanthones are identified as novel, non-toxic VSMC proliferation inhibitors, which might contribute to the development of new therapeutic applications to combat restenosis.
Journal of Natural Products | 2017
Rongxia Liu; Elke H. Heiss; Daniel Schachner; Baohong Jiang; Wanhui Liu; Johannes M. Breuss; Verena M. Dirsch; Atanas G. Atanasov
Xanthohumol (1) is a principal prenylated chalcone found in hops. The aim of this study was to examine its influence on platelet-derived growth factor (PDGF)-BB-triggered vascular smooth muscle cell (VSMC) proliferation and migration in vitro and on experimentally induced neointima formation in vivo. Quantification of resazurin conversion indicated that 1 can inhibit PDGF-BB-induced VSMC proliferation concentration-dependently (IC50 = 3.49 μM). Furthermore, in a wound-healing assay 1 potently suppresses PDGF-BB-induced VSMC migration at 15 μM. Tested in a mouse femoral artery cuff model, 1 significantly reduces neointima formation. Taken together, we show that 1 represses PDGF-BB-induced VSMC proliferation and migration in vitro as well as neointima formation in vivo. This novel activity suggests 1 as an interesting candidate for further studies addressing a possible therapeutic application to counteract vascular proliferative disease.
F1000Research | 2015
Rongxia Liu; Elke H. Heiss; Dean Guo; Verena M. Dirsch; Atanas G. Atanasov
Accelerated vascular smooth muscle cell (VSMC) proliferation is implied in cardiovascular disease and significantly contributes to vessel lumen reduction following surgical interventions such as percutaneous transluminal coronary angioplasty or bypass surgery. Therefore, identification and characterization of compounds and mechanisms able to counteract VSMC proliferation is of potential therapeutic relevance. This work reveals the anti-proliferative effect of the natural product capsaicin from Capsicum spp. by quantification of metabolic activity and DNA synthesis in activated VSMC. The observed in vitro activity profile of capsaicin warrants further research on its mechanism of action and potential for therapeutic application.
Molecular Nutrition & Food Research | 2018
Rongxia Liu; Elke H. Heiss; Birgit Waltenberger; Tina Blažević; Daniel Schachner; Baohong Jiang; Vladimír Kryštof; Wanhui Liu; Stefan Schwaiger; Luis M. Peña-Rodríguez; Johannes M. Breuss; Hermann Stuppner; Verena M. Dirsch; Atanas G. Atanasov
Planta Medica | 2016
Christina E. Mair; Rongxia Liu; Atanas G. Atanasov; M Schmidtke; Verena M. Dirsch; Judith M. Rollinger
Planta Medica | 2015
Birgit Waltenberger; Rongxia Liu; Atanas G. Atanasov; Stefan Schwaiger; Elke H. Heiss; Vm Dirsch; Hermann Stuppner