Objective To investigate the effect of daphnetin on superoxide dismutase (SOD) activity and DNA synthesis in P. falciparum in vitro. Methods The effect of daphnetin, daphnetin-Fe complex and desferrioxamine B on SOD activity of P. falciparum (P. f) FOCI in vitro was determined with a SOD test-kit. The level of DNA synthesis of P. f synchronized cultured in vitro at various developmental stages after treatment of daphnetin or desferrioxamine B was assayed by fluorescein Hoechest 33258. Results The total SOD activity decreased by 60% after daphnetin treatment while it only decreased by 22% if treated with desferrioxamine B. No effect on SOD activity of P. f treated with daphnetin-Fe complex was observed. The level of DNA synthesis of P. f trophozoites in synchronized in vitro culture was significantly lower than that of the control. Conclusion Daphnetin lowered SOD activity and decreased DNA synthesis of P. f in vitro.

Objective To investigate the therapeutic effect of a combination of artemether and daphnetin against Plasmodium berghei ANKA strain in mice. Methods Groups of P. berghei infected mice were treated with various oral doses of artemether and daphnetin according to “4-day suppress assay”. Thin blood smears were made on the fifth day after inoculation of parasites and the parasitemia reduction rate was calculated. The ED 50 values obtained were plotted on isobolograms. A combined action of artemether and daphnetin was assessed. Results Artemether 0.4mg/(kg?d)?4d exhibited no detectable antimalarial effect, while artemether 0.4mg/(kg?d)?4d combined with daphnetin 7.7 mg/kg.d?4d showed potent antiparasile efficacy. The ED 50s of artemether in combination with daphnetin were lower than that of single artemether or daphnetin. The R-values were higher than 0.4, but lower than 2.7. Conclusion The combination of artemether with daphnetin showed an additive antiparasile effect.

In order to investigate the transfer and expression of Snail gene in human bone mesenchymal stem cells (MSCs) and to study effects of Snail gene modification on the CXCR4 expression of human MSCs and their capacity of migration to SDF-1 in vitro, the plasmid PCAGGSneo-Snail-HA or the control vector of PCAGGSneo was transferred into the cells. Fluorescence activated cell sorting analysis, immunofluorescence staining and RT-PCR were used to study the expression of CXCR4 by MSCs. Chemotaxis assays were performed to evaluate the migratory capacity of MSCs-Sna and MSCs-neo to SDF-1 in vitro. For the blocking assay, CXCR4 blocking antibody was added into cell culture. CXCR4 expression was higher in MSCs-Sna than that in MSCs-neo (P < 0.05). Chemotaxis assays showed that SDF-1alpha stimulated migratory activity of MSCs-Sna more than MSCs-neo in vitro (P < 0.05). Moreover, the SDF-1alpha-induced migratory activity of MSCs-Sna was inhibited in a concentration-dependent manner by a CXCR4-blocking antibody. It was concluded that Snail enhanced expression of CXCR4 in MSCs, providing a plausible mechanism for Snail-mediated MSCs transmigration to damaged tissues in vivo where SDF-1 has been shown to be up-regulated as part of injury responses.
Bone Marrow Cells ; cytology ; Cell Movement ; genetics ; Cells, Cultured ; Chemokine CXCL12 ; metabolism ; Humans ; Mesenchymal Stromal Cells ; cytology ; metabolism ; Receptors, CXCR4 ; genetics ; metabolism ; Snail Family Transcription Factors ; Transcription Factors ; genetics ; Transduction, Genetic