BackgroundSevere anaemia due to dyserythropoiesis has been documented in patients infected with Plasmodium vivax, however the mechanism responsible for anaemia in vivax malaria is poorly understood. In order to better understand the role of P. vivax infection in anaemia the inhibition of erythropoiesis using haematopoietic stem cells was investigated.MethodsHaematopoietic 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 P. vivax parasites either from intact or lysed infected erythrocytes (IE) was examined for the effect on inhibition of cell development compared with untreated controls.ResultsBoth 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 P. vivax on cell expansion. Exposure to P. vivax 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 (P-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 P. vivax, indicating that impaired erythropoiesis was independent of these cytokines.ConclusionsThis study shows for the first time that P. vivax parasites inhibit erythroid development leading to ineffective erythropoiesis and highlights the potential of P. vivax to cause severe anaemia.

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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.

Colorectal cancer (CRC) is an aggressive malignancy. Critical mechanisms that support CRC progression include cell migration, invasion, metastasis, and angiogenesis, which is associated with L1 cell adhesion molecule (L1CAM) and nuclear factor-kappa B (NF-κB) signaling pathways. In this study, viability of HT-29 cells and human umbilical vein endothelial cells (HUVECs) was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, and cell apoptosis was investigated by flow cytometry assays. HT-29 cell migration and invasion were observed by wound healing and Transwell invasion assays, respectively, and tube formation of HUVECs was observed by tubulogenesis assays. L1CAM and NF-κB protein expressions in HT-29 cells treated with onion peel extract were determined by indirect immunofluorescence. Results showed that high dose treatments of onion peel extract inhibited cell viability of both HT-29 cells and HUVECs, induced HT-29 cell apoptosis, and inhibited HT-29 cell migration and invasion. Moreover, onion peel extract decreased total HUVEC tube length and, at a concentration of 10 μg/mL, showed potential to downregulate L1CAM and NF-κB. In conclusion, onion peel extract inhibits HT-29 cell growth, migration, and invasion through suppressing pathways related to angiogenesis downstream of L1CAM-activated NF-κB.

Ultraviolet type B (UVB) radiation plays an important role in hyperpigmentation disorder, which induces cellular oxidative stress and causes abnormal melanin production and secretion. The stress condition plays an essential role in actin polymerization relating to F-actin rearrangement and forms dendrite to send melanin pigment to the uppermost layer of the skin. Phenolic compounds are secondary metabolites that mainly synthesize under stress conditions to protect plants from harmful environments and have been reported as effective agents in anti-oxidant and anti-melanogenesis. However, the influence of phenolic compounds on F-actin rearrangement-associated dendrite formation has not been studied so far. Hence, this study aimed to investigate the enhancing phytophenolic targets in riceberry rice (Oryza sativa L.) germination and UVB radiation (RR-GR) to suppress melanogenesis relating to F-rearrangement. As a result, the RR-GR had the potential to enhance phenolic acids such as protocatechuic and vanillic acid, which have been proven to possess anti-oxidant activity and anti-tyrosinase properties. Riceberry rice’s modification showed the potential to reduce cellular oxidative stress and suppress B16F10 melanogenesis relating to F-actin rearrangement that is associated with dendrite formation.