Abstract Anthocyanin/polyvinyl alcohol/chitosan composite membrane was prepared by solution casting method using chitosan (CS) and polyvinyl alcohol (PVA) as matrix and natural pigment anthocyanin as filler. The structures of the composite films were characterized by Uv-visible reflectance spectrum (UV-VIS), Fourier infrared spectroscopy (FT-IR) and the scanning electron microscopy (SEM). The effects of adding anthocyanins on the physical properties, water resistance, degradation, antibacterial properties and pH responsiveness of the films were investigated. The experimental results showed that the prepared anthocyanin/polyvinyl alcohol/chitosan composite indicator films show color changes from pink to purple to blue and then to yellow-green when the pH value ranges from 2 to 14. The total color difference ΔE value is greater than 12. The antibacterial properties and other properties of the composite film can enhance by adding anthocyanin. The tensile strength of anthocyanin/polyvinyl alcohol/chitosan film is more than 70 MPa, which is larger than that of polyvinyl film and polyvinyl alcohol/chitosanfilm. The film has excellent physical, antibacterial properties and obvious pH response performance, making it ideal for food packaging.

Although Taxol has improved the survival of cancer patients as a first-line chemotherapeutic agent, an increasing number of patients develop resistance to Taxol after prolonged treatment. The potential mechanisms of cancer cell resistance to Taxol are not completely clear. It has been reported that microRNAs (miRNAs) are involved in regulating the sensitivity of cancer cells to various chemotherapeutic agents. In this study, we aimed to explore the role of miR-129-5p in regulating the sensitivity of breast cancer cells to Taxol. Cell apoptosis and autophagy, and the sensitivity of MCF-7 cells to Taxol were assessed with a series of in vitro assays. Our results showed that the inhibition of autophagy increased the Taxol-induced apoptosis and the sensitivity of MCF-7 cells to Taxol. Up-regulation of miR-129-5p also inhibited autophagy and induced apoptosis. Furthermore, miR-129-5p overexpression increased the sensitivity of MCF-7 cells to Taxol. High mobility group box 1 (HMGB1), a target gene of miR-129-5p and a regulator of autophagy, was negatively regulated by miR-129-5p. We found that interference of HMGB1 enhanced the chemosensitivity of Taxol by inhibiting autophagy and inducing apoptosis in MCF-7 cells. Taken together, our findings suggested that miR-129-5p increased the chemosensitivity of MCF-7 cells to Taxol through suppressing autophagy and enhancing apoptosis by inhibiting HMGB1. Using miR-129-5p/HMGB1/autophagy-based therapeutic strategies may be a potential treatment for overcoming Taxol resistance in breast cancer.

A simple and effective salting-out method was developed for the purification of the metallo-β-lactamase CcrA from Bacteroides fragilis based on the plasmid pMSZ02, in which the crude protein secreted into growth medium was precipitated by 80% sulfate saturation of the medium and purified with Q-Sepharose to offer pure CcrA with yield of 20.1 mg per litter medium. The dependence of the amount of protein precipitation on sulfate saturation was investigated, which showed that more than 80% sulfate saturation resulted the maximum protein precipitated. The purified CcrA was evaluated by steady-state kinetics using penicillin G and cephalothin V as substrates, which showed the Km values of 68±2 and 17±2 µM and Kcat values of 63±1 and 102±3 S-1, respectively. The comparison with the data of the protein from literature method showed that the salting-out method was viable, and it could be useful for the purification of other proteins secreted into growth medium.

Abnormal genome hypermethylation participates in the tumorigenesis and development of prostate cancer. Prostate cancer cells highly express DNA methyltransferase 3 (DMNT3) family genes, essential for maintaining genome methylation. In the present study, multi-target siRNA, based on the homologous region of the DNMT3 family, was designed for the in vitro investigation of its effects on the proliferation, migration, and invasion of TSU-PR1 prostate cancer cells. The consequential cell-cycle derangement, through DNMT3A/B or only DNMT3B silencing, was partially efficient, without affecting apoptosis. DNMT3A silencing had absolutely no effect on changing TSU-PR1 cell biological behavior. Hence, DNMT3B alone apparently plays a key role in maintaining the unfavorable behavior of prostate-cancer cells, thereby implying its potential significance as a promising therapeutic target, with DNMT3A simply in the role of helper.