Nymphaea pubescens Induces Apoptosis, Suppresses Cellular Oxidants-Related Cell Invasion in B16 Melanoma Cells

Background: Nymphaea spp., Thai water lilies are aquatic plants. They contain phenolic pigments that play a major role in free radical scavenging. Melanoma is strong aggressive skin cancer-associated with oxidative stress. This study, to determine the effect of Nymphaea spp. extracts on cell apoptosis, cellular migration and invasion through the role of cellular oxidants in B16 melanoma cells. Methods: Free radical scavenging activity and total phenolic were investigated by 1, 1-diphenyl-2 picrylhydrazyl (DPPH) and Ferric reducing anti-oxidant power (FRAP) methods and Folin-Denis test, respectively. Cytotoxic were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method. Cell apoptosis was confirmed by flow cytometry. Cellular oxidants, cellular migration and invasion were determined with 2,7-dichlorodihydrofluorescein diacetate (DCFH-DA), wound healing and Boyden chamber assay, respectively. Results: Nymphaea pubescens showed higher capacity of scavenging free radical activity than Nymphaea stellate and also related phenolic content. Nymphaea pubescens extract was toxic to B16 melanoma cells. High concentrations cell apoptosis was induced. Contrastingly, low concentrations showed a decrease in cellular oxidants associated with the suppression of cancer cell progression. In B16 melanoma cell, Nymphaea pubescens extract was able to inhibit B16 melanoma cell migration and invasion through the low doses. Interestingly, the high doses of extract showed a potential of cytotoxicity to induce melanoma cell death. At the low doses, Nymphaea pubescens extract might suppress melanoma cells progression by interfering with both cellular migration and invasion capacity. Conclusion: Hence, Nymphaea pubescens extract induced cellular apoptosis and it also suppressed cancer cell progression by reducing oxidative stress in B16 melanoma cells

Quercetin Inhibits Colorectal Cancer Cells Induced-Angiogenesis in Both Colorectal Cancer Cell and Endothelial Cell through Downregulation of VEGF-A/VEGFR2

Colorectal cancer (CRC) aggressiveness is caused by cancer angiogenesis which promotes the cancer growth and metastasis associated with poor prognosis and poor survival. The vascular endothelial growth factor-A (VEGF-A) and its receptor (VEGFR-2) form the major signaling pathway in cancer angiogenesis. This study aimed to investigate the anti-angiogenesis activity of quercetin in both colorectal cancer cells and endothelial cells. The tube formation of human vein endothelial cells (HUVECs) was determined by using conditioned media of HT-29 cells treated with quercetin co-cultured with HUVECs. The VEGF-A and NF-κB p65 protein expressions in the quercetin-treated HT-29 cells were determined by fluorescence assay and Western blot analysis. The VEGFR-2 protein expression in HUVECs was determined after they were co-cultured with the quercetin-treated HT-29 cells. Quercetin markedly decreased the HT-29 cell-induced angiogenesis in HUVECs. NF-κB p65 and VEGF-A protein expression were also inhibited by quercetin. Moreover, quercetin significantly inhibited VEGFR-2 expression and translocation in HUVECs after they were co-cultured with high dose quercetin-treated HT-29 cells. Taken together, quercetin had an anti-angiogenesis effect on VEGF-A inhibition related to the NF-κB signaling pathway in the HT-29 cells and reduced VEGFR-2 expression and translocation in HUVECs

Suppression of erythroid development <it>in vitro</it> by <it>Plasmodium vivax</it>

<p>Abstract</p> <p>Background</p> <p>Severe anaemia due to dyserythropoiesis has been documented in patients infected with <it>Plasmodium vivax,</it> however the mechanism responsible for anaemia in vivax malaria is poorly understood. In order to better understand the role of <it>P. vivax</it> infection in anaemia the inhibition of erythropoiesis using haematopoietic stem cells was investigated.</p> <p>Methods</p> <p>Haematopoietic stem cells/CD34⁺ cells, isolated from normal human cord blood were used to generate growing erythroid cells. Exposure of CD34⁺ cells and growing erythroid cells to <it>P. vivax</it> parasites either from intact or lysed infected erythrocytes (IE) was examined for the effect on inhibition of cell development compared with untreated controls.</p> <p>Results</p> <p>Both lysed and intact infected erythrocytes significantly inhibited erythroid growth. The reduction of erythroid growth did not differ significantly between exposure to intact and lysed IE and the mean growth relative to unexposed controls was 59.4 ± 5.2 for lysed IE and 57 ± 8.5% for intact IE. Interestingly, CD34⁺ cells/erythroid progenitor cells were susceptible to the inhibitory effect of <it>P. vivax</it> on cell expansion. Exposure to <it>P. vivax</it> also inhibited erythroid development, as determined by the reduced expression of glycophorin A (28.1%) and CD 71 (43.9%). Moreover, vivax parasites perturbed the division of erythroid cells, as measured by the Cytokinesis Block Proliferation Index, which was reduced to 1.35 ± 0.05 (<it>P</it>-value < 0.01) from a value of 2.08 ± 0.07 in controls. Neither TNF-a nor IFN-g was detected in the culture medium of erythroid cells treated with <it>P. vivax,</it> indicating that impaired erythropoiesis was independent of these cytokines.</p> <p>Conclusions</p> <p>This study shows for the first time that <it>P. vivax</it> parasites inhibit erythroid development leading to ineffective erythropoiesis and highlights the potential of <it>P. vivax</it> to cause severe anaemia.</p