The Fe-doped TiO2nanocomposites synthesized by a deposition-precipitation method were characterized by X-ray diffraction (XRD), transmission electron microscope (TEM), X-ray photoelectron spectroscopy (XPS), and UV-vis adsorption spectra and then were taken as a new “photosensitizer” for photodynamic therapy (PDT). The photocatalytic inactivation of Fe-doped TiO2on Leukemic HL60 cells was investigated using PDT reaction chamber based on LED light source, and the viability of HL60 cells was examined by Cell Counting Kit-8 (CCK-8) assay. The experimental results showed that the growth of leukemic HL60 cells was significantly inhibited by adding TiO2nanoparticles, and the inactivation efficiency could be effectively enhanced by the surface modification of TiO2nanoparticles with Fe doping. Furthermore, the optimized conditions were achieved at 5 wt% Fe/TiO2at a final concentration of 200 μg/mL, in which up to 82.5% PDT efficiency for the HL60 cells can be obtained under the irradiation of 403 nm light (the power density is 5 mW/cm2) within 60 minutes.

The Fe-N co-doped TiO2nanocomposites were synthesized by a sol-gel method and characterized by scanning electron microscope (SEM), transmission electron microscope (TEM), X-ray diffraction (XRD), ultraviolet-visible absorption spectroscopy (UV-vis) and X-ray photoelectron spectroscopy (XPS). Then the photocatalytic inactivation of Fe-N-doped TiO2on leukemia tumors was investigated by using Cell Counting Kit-8 (CCK-8) assay. Additionally, the ultrastructural morphology and apoptotic percentage of treated cells were also studied. The experimental results showed that the growth of leukemic HL60 cells was significantly inhibited in groups treated with TiO2nanoparticles and the photocatalytic activity of Fe-N-TiO2was significantly higher than that of Fe-TiO2and N-TiO2, indicating that the photocatalytic efficiency could be effectively enhanced by the modification of Fe-N. Furthermore, when 2 wt% Fe-N-TiO2nanocomposites at a final concentration of 200 μg/mL were used, the inactivation efficiency of 78.5% was achieved after 30-minute light therapy.

Background/Aims: P-glycoprotein (P-gp, i.e., MDR1) is associated with the phenotype of multidrug resistance (MDR) and causes chemotherapy failure in the management of cancers. Searching for effective MDR modulators and combining them with anticancer drugs is a promising strategy against MDR. Asiatic acid (AA), a natural triterpene isolated from the plant Centella asiatica, may have an antitumor activity. The present study assessed the reversing effect of AA on MDR and possible molecular mechanisms of AA action in MDR1-overexpressing cisplatin (DDP)-resistant lung cancer cells, A549/DDP. Methods: Human lung adenocarcinoma A549/DDP cells were either exposed to different concentrations of AA or treated with DDP, and their viability was measured by the MTT assay. A Rhodamine 123 efflux assay, immunofluorescent staining, ATPase assay, reverse-transcription PCR (RT-PCR), and western blot analysis were conducted to elucidate the mechanisms of action of AA on MDR. Results: Our results showed that AA significantly enhanced the cytotoxicity of DDP toward A549/DDP cells but not its parental A549 cells. Furthermore, AA strongly inhibited P-gp expression by blocking MDR1 gene transcription and increased the intracellular accumulation of the P-gp substrate Rhodamine 123 in A549/DDP cells. Nuclear factor (NF)-kB (p65) activity, IkB degradation, and NF-kB/p65 nuclear translocation were markedly inhibited by pretreatment with AA. Additionally, AA inhibited the MAPK–ERK pathway, as indicated by decreased phosphorylation of ERK1 and -2, AKT, p38, and JNK, thus resulting in reduced activity of the Y-box binding protein 1 (YB1) via blockage of its nuclear translocation. Conclusions: AA reversed P-gp-mediated MDR by inhibition of P-gp expression. This effect was likely related to downregulation of YB1, and this effect was mediated by the NF-kB and MAPK–ERK pathways. AA may be useful as an MDR reversal agent for combination therapy in clinical trials.

Microfluidic chips are generally fabricated by a soft lithography method employing commercial lithography equipment. These heavy machines require a critical room environment and high lamp power, and the cost remains too high for most normal laboratories. Here we present a novel microfluidics fabrication method utilizing a portable ultraviolet (UV) LED as an alternative UV source for photolithography. With this approach, we can repeat several common microchannels as do these conventional commercial exposure machines, and both the verticality of the channel sidewall and lithography resolution are proved to be acceptable. Further microfluidics applications such as mixing, blood typing and microdroplet generation are implemented to validate the practicability of the chips. This simple but innovative method decreases the cost and requirement of chip fabrication dramatically and may be more popular with ordinary laboratories.

We describe a cheap, easily assembled, controllable droplet fission device to obtain a variety of uniform daughter droplets.