Matrine inhibits hepatocellular carcinoma cell malignancy through the circ_0013290/miR-139-5p/MMP16 pathway

Background. Previous studies have shown the anticancer effect of Matrine on hepatocellular carcinoma (HCC); however, the underlying mechanism is still indistinct. Methods. The expression of circular RNA_0013290 (circ_0013290), microRNA-139-5p (miR-139-5p), matrix metallopeptidase 16 (MMP16), CyclinD1 and N-cadherin was analyzed by quantitative real-time polymerase chain reaction, Western blotting or immuno-histochemistry assay. Cell viability, proliferation, apoptosis, invasion and tube formation were analyzed by cell counting kit-8, 5-Ethynyl-2’-deoxyuridine, flow cytometry analysis, transwell invasion and tube formation assays, respectively. The associations among circ_0013290, miR-139-5p and MMP16 were predicted by starbase online database, and identified by dual-luciferase reporter and RNA pull-down assays. A xenograft mouse model assay was conducted to disclose the effects of circ_0013290 and Matrine on tumor tumorigenesis in vivo. Results. Circ_0013290 and MMP16 expression were significantly upregulated, while miR-139-5p was downregulated in HCC tissues and cells compared with the matched normal liver tissues and cells. Matrine treatment inhibited HCC cell proliferation, invasion and tube formation but induced cell apoptosis, accompanied by the decrease of CyclinD1 and N-cadherin expression; however, these effects were counteracted when circ_0013290 expression was increased. MiR-139-5p depletion or MMP16 introduction relieved Matrine-induced effects in HCC cells. The regulation of circ_0013290 toward HCC cell processes involved MMP16. With respect to the mechanism, circ_0013290 acted as a miR-139-5p sponge, and miR-139-5p targeted MMP16 in HCC cells. Besides, circ_0013290 regulated MMP16 expression through miR-139-5p. Further, circ_0013290 depletion enhanced the inhibitory effects of Matrine on tumor tumorigenesis. Conclusion. Matrine inhibited HCC cell malignancy through the circ_0013290/miR-139-5p/MMP16 pathway, suggesting that Matrine is a potential therapeutic agent for HC

Styrene-assisted maleic anhydride grafted poly(lactic acid) as an effective compatibilizer for wood flour/poly(lactic acid) bio-composites

This study aimed to evaluate the effect of styrene-assisted maleic anhydride-grafted poly(lactic acid) (PLA-g-St/MAH) on the interfacial properties of wood flour/poly(lactic acid) (PLA) bio-composites. PLA-g-St/MAH was synthesized by free-radical melt grafting using styrene as a comonomer and dicumyl peroxide as an initiator. The structure of PLA-g-St/MAH was characterized by Fourier transform infrared spectroscopy. Wood flour/PLA composites were prepared by compression molding using PLA-g-St/MAH as a compatibilizer. The effects of PLA-g-St/MAH on the rheological and mechanical properties, as well as on the fractured surface morphology of the composites were investigated. Results indicated that storage modulus, complex viscosity, equilibrium torque, and shear heat were significantly increased. The mechanical properties of the wood flour/PLA composites were also significantly increased after the addition of PLA-g-St/MAH. The maximum values were achieved at the loading rate of 3 wt % because of the improved interfacial adhesion between the wood flour and the PLA matrix

High performance Bi2Te3 nanocomposites prepared by single-element-melt-spinning spark-plasma sintering

The last decade has witnessed nanocomposites becoming a new paradigm in the field of thermoelectric (TE) research. At its core is to prepare high performance TE nanocomposites, both p- and n-type, in a time and energy efficient way. To this end, we in this article summarize our recent effort and results on both p- and n-type Bi2Te3-based nanocomposites prepared by a unique single-element-melt-spinning spark-plasma sintering procedure. The results of transport measurements, scanning and transmission electronic microscopy, and small angle neutron scattering have proved essential in order to establish the correlation between the nanostructures and the TE performance of the materials. Interestingly, we find that in situ formed nanocrystals with coherent boundaries are the key nanostructures responsible for the significantly improved TE performance of p-type Bi2Te3 nanocomposites whereas similar nanostructures turn out to be less effective for n-type Bi2Te3 nanocomposites. We also discuss the alternative strategies to further improve the TE performance of n-type Bi2Te3 materials via nanostructuring processe

Inhibition of HSP90 promotes neural stem cell survival from oxidative stress through attenuating NF-κB/p65 activation

Stem cell survival post transplantation determines the efficiency of stem cell treatment, which develops as a novel potential therapy for several central nervous system (CNS) diseases in recent decades of yeas. The engrafted stem cells face the damage of oxidative stress, inflammation and immune response at the lesion point in host. Among the pathology, oxidative stress directs stem cells to apoptosis and even death through several signalling pathways and DNA damage. However, the in detail mechanism of stem cell survival from oxidative stress has not revealed clearly. Here in this study, we used hydrogen peroxide (H2O2) to induced the oxidative damage on neural stem cells (NSCs). The damage was in consequence demonstrated involving the activation of heat shock protein 90 (HSP90) and NF-κB/p65 signalling pathways. Further application of the pharmacological inhibitors respectively targeting at each signalling indicated an upper streaming role of HSP90 upon NF-κB/p65 on NSCs survival. Pre-inhibition of HSP90 with the specific inhibitor displayed a significant protection on NSCs against oxidative stress. In conclusion, inhibition of HSP90 would attenuate NF-κB/p65 activation by oxidative induction and promote NSCs survival from oxidative damage. The HSP90/NF-κB mechanism provides a new evidence on rescuing NSCs from oxidative stress, and also promotes the stem cell application on CNS pathologies

Inhibition of HSP90 Promotes Neural Stem Cell Survival from Oxidative Stress through Attenuating NF- κ

Stem cell survival after transplantation determines the efficiency of stem cell treatment, which develops as a novel potential therapy for several central nervous system (CNS) diseases in recent decades. The engrafted stem cells face the damage of oxidative stress, inflammation, and immune response at the lesion point in host. Among the damaging pathologies, oxidative stress directs stem cells to apoptosis and even death through several signalling pathways and DNA damage. However, the in-detail mechanism of stem cell survival from oxidative stress has not been revealed clearly. Here, in this study, we used hydrogen peroxide (H2O2) to induce the oxidative damage on neural stem cells (NSCs). The damage was in consequence demonstrated involving the activation of heat shock protein 90 (HSP90) and NF-κB/p65 signalling pathways. Further application of the pharmacological inhibitors, respectively, targeting at each signalling indicated an upper-stream role of HSP90 upon NF-κB/p65 on NSCs survival. Preinhibition of HSP90 with the specific inhibitor displayed a significant protection on NSCs against oxidative stress. In conclusion, inhibition of HSP90 would attenuate NF-κB/p65 activation by oxidative induction and promote NSCs survival from oxidative damage. The HSP90/NF-κB mechanism provides a new evidence on rescuing NSCs from oxidative stress and also promotes the stem cell application on CNS pathologies

3D-printed polycaprolactone-chitosan based drug delivery implants for personalized administration

Fused deposition molding (FDM) can complete most complex preparation of drug delivery implants to meet the personalized needs of patients. However, the drug activity has strict requirements on processing temperature and preparation method of filaments, the implant also has strict biocompatibility requirements for the materials. In this study, a drug delivery implant was prepared with good biocompatibility, controlled and efficient drug release using FDM printing for personalized administration. Drug-loaded filaments were developed for FDM process by hot-melt extrusion (HME). Polycaprolactone was used as a drug delivery carrier, and ibuprofen as the model drug. Notably, chitosan was dissolved to form controlled and efficient release channels. The printability, changes in physical and chemical properties during HME and FDM processes of the filament, and drug release behavior, mechanism and biocompatibility of the implants were investigated. The results showed that the filament tensile strength decreased with the increase of drug and chitosan content. No obvious degradation and chemical change occurred during the whole process. The drug release efficiency could reach\u3e99% and lasted for 120 h mainly via the diffusion - erosion mechanism. The viability of cells cultured for 24 h in 72 h, 100% implant extract was 75.3%

High-purity recycling of hematite and Zn/Cu mixture from waste smelting slag

In this study, Zn/Cu-bearing smelting slag was recycled via an integrated acid dissolution and hematite precipitation method. The slag was dissolved in nitric acid to generate an acid solution containing 23.5 g/L Fe, 4.45 g/L Zn and 2.81 g/L Cu, which was subjected to hydrothermal treatment with the addition of levulinic acid (LA). More than 99.95% of the initial Fe content was removed as hematite particles with diameters of approximately 200 nm, and the residual Fe concentration in the acid was 0.43 mg/L. The generated hematite contained 97.3% Fe2O3, 0.64% ZnO and 0.58% CuO. Greater than 99% of the initial Zn and Cu was retained in the acid and further precipitated as Zn/Cu-bearing solids by adjusting the solution pH to 9. The precipitated Zn/Cu-bearing solids contained 33.6% Zn and 21.7% Cu, whereas the Fe content was less than 0.2%. This paper is the first report of an environmentally friendly approach for recycling smelting slag without generating any hazardous waste

Inhibition of HSP90 promotes neural stem cell survival from oxidative stress through attenuating NF-κB/p65 activation

Stem cell survival post transplantation determines the efficiency of stem cell treatment, which develops as a novel potential therapy for several central nervous system (CNS) diseases in recent decades of yeas. The engrafted stem cells face the damage of oxidative stress, inflammation and immune response at the lesion point in host. Among the pathology, oxidative stress directs stem cells to apoptosis and even death through several signalling pathways and DNA damage. However, the in detail mechanism of stem cell survival from oxidative stress has not revealed clearly. Here in this study, we used hydrogen peroxide (H2O2) to induced the oxidative damage on neural stem cells (NSCs). The damage was in consequence demonstrated involving the activation of heat shock protein 90 (HSP90) and NF-κB/p65 signalling pathways. Further application of the pharmacological inhibitors respectively targeting at each signalling indicated an upper streaming role of HSP90 upon NF-κB/p65 on NSCs survival. Pre-inhibition of HSP90 with the specific inhibitor displayed a significant protection on NSCs against oxidative stress. In conclusion, inhibition of HSP90 would attenuate NF-κB/p65 activation by oxidative induction and promote NSCs survival from oxidative damage. The HSP90/NF-κB mechanism provides a new evidence on rescuing NSCs from oxidative stress, and also promotes the stem cell application on CNS pathologies