Synergistic Therapy of Doxorubicin with Cationic Anticancer Peptide L-K6 Reverses Multidrug Resistance in MCF-7/ADR Cancer Cells In Vitro via P-glycoprotein Inhibition

International Journal of Peptide Research and Therapeutics - Multidrug resistance (MDR) is one of the major obstacles to efficient chemotherapy against cancers, resulting from the overexpression of...     

Contribution of P2X4 receptor in pain associated with rheumatoid arthritis: a review

Purinergic Signalling - Pain is the most common symptom reported by patients with rheumatoid arthritis (RA) even after the resolution of chronic joint inflammation. It is believed that...     

Enzymatic deinking of various types of waste paper: Efficiency and characteristics

The aim of the present study was to characterize the enzymatic deinking of various types of waste paper. Studies on the optimization of enzymatic deinking have been performed previously using commercially available enzyme preparations containing cellulase and hemicellulase. The enzymatic deinking of different types of waste paper demonstrated a high efficiency of 86.6% on laser-printed paper, but a low deinking efficiency of 12.9% was obtained with newspaper. All enzymatic treatments significantly improved the drainage rate of the deinked waste paper. Enzymatic deinking increased the tensile index of magazine paper but reduced the tensile index of bubble jet-printed paper, photocopy paper and newspaper. Enzymatic hydrolysis caused a 21.1% reduction in the tear index for bubble jet-printed paper, but a 3.1% increase in the tear index was obtained for laser-printed paper relative to respective blank. In addition, enzymatic hydrolysis increased the burst index by 4.7% relative to blank for laser-printed paper. However, photocopy paper showed the highest reduction (8.3%) in the burst index relative to blank. Taken together, these results suggest that enzymatic hydrolysis is both advantageous and detrimental to the mechanical properties of deinked paper. Thus, the proper regulation of enzymatic hydrolysis is crucial to improve the quality of recycled paper.     

One‐Step Fabrication of Ultrathin Porous Nickel Hydroxide‐Manganese Dioxide Hybrid Nanosheets for Supercapacitor Electrodes with Excellent Capacitive Performance

A facile one‐step hydrothermal co‐deposition method for growth of ultrathin Ni(OH)₂‐MnO₂ hybrid nanosheet arrays on three dimensional (3D) macroporous nickel foam is presented. Due to the highly hydrophilic and ultrathin nature of hybrid nanosheets, as well as the synergetic effects of Ni(OH)₂ and MnO₂, the as‐fabricated Ni(OH)₂‐MnO₂ hybrid electrode exhibits an ultrahigh specific capacitance of 2628 F g^?1. Moreover, the asymmetric supercapacitor with the as‐obtained Ni(OH)₂‐MnO₂ hybrid film as the positive electrode and the reduced graphene oxide as the negative electrode has a high energy density (186 Wh kg^?1 at 778 W kg^?1), based on the total mass of active materials.     

Phenylpropanoid constituents from the seeds of Lithocarpus pachylepis

Five phenylpropanoids including one new compound balanophonin A (1), one new natural compound balanophonin B (2) were isolated from the seeds of Lithocarpus pachylepis for the first time. Their structures were elucidated by various spectroscopic techniques (UV, IR, MS, CD, 1D and 2D NMR). All compounds were evaluated for their anti-inflammatory activities on lipopolysaccharide (LPS)-induced nitric oxide (NO) production in RAW 264.7.     

A Novel Anti-Tumor Inhibitor Identified by Virtual Screen with PLK1 Structure and Zebrafish Assay

Polo-like kinase 1 (PLK1), one of the key regulators of mitosis, is a target for cancer therapy due to its abnormally high activity in several tumors. Plk1 is highly conserved and shares a nearly identical 3-D structure between zebrafish and humans. The initial 10 mitoses of zebrafish embryonic cleavages occur every∼30 minutes, and therefore provide a rapid assay to evaluate mitosis inhibitors including those targeting Plk1. To increase efficiency and specificity, we first performed a computational virtual screen of∼60000 compounds against the human Plk1 3-D structure docked to both its kinase and Polo box domain. 370 candidates with the top free-energy scores were subjected to zebrafish assay and 3 were shown to inhibit cell division. Compared to general screen for compounds inhibiting zebrafish embryonic cleavage, computation increased the efficiency by 11 folds. One of the 3 compounds, named I2, was further demonstrated to effectively inhibit multiple tumor cell proliferation in vitro and PC3 prostate cancer growth in Xenograft mouse model in vivo. Furthermore, I2 inhibited Plk1 enzyme activity in a dose dependent manner. The IC₅₀ values of I2 in these assays are compatible to those of ON-01910, a Plk1 inhibitor currently in Phase III clinic trials. Our studies demonstrate that zebrafish assays coupled with computational screening significantly improves the efficiency of identifying specific regulators of biological targets. The PLK1 inhibitor I2, and its analogs, may have potential in cancer therapeutics.     

Retracted: Upregulated microRNA-31 inhibits oxidative stress-induced neuronal injury through the JAK/STAT3 pathway by binding to PKD1 in mice with ischemic stroke

Ischemic stroke (IS), which is characterized by high morbidity, disability, and mortality, is recognized as a major cerebrovascular disease. MicroRNA-31 (miR-31) was reported to participate in the progression of brain disease. The present study was conducted in order to investigate the effect of miR-31 on oxidative stress-induced neuronal injury in IS mice with the involvement of protein kinase D1 (PKD1) and the JAK/STAT3 pathway. C57BL/6J mice were used to establish the middle cerebral artery occlusion (MCAO) model. Astrocytes were transfected with miR-31 mimic, miR-31 inhibitor, si-PKD1, or JAK-STAT3 pathway inhibitor. Following the establishment of an oxygen–glucose deprivation (OGD) model, the astrocytes were cocultured with neuronal OGD. Lower miR-31, higher PKD1 expressions, and activated JAK/STAT3 pathway were found in both the MCAO and OGD models. miR-31 could negatively target PKD1. In an MCAO model, overexpressing miR-31 and silencing PKD1 reduced neuronal injury, cerebral infarct volume, neuron loss, and oxidative stress injury, inhibited the activation of JAK/STAT3 pathway and the expressions of PKD1, interleukin (IL)-1β, IL-6, tumor necrosis factor-α, malondialdehyde, 4-HNE, 8-HOdG, caspase-3, and Bax, but increased the superoxide dismutase content. In the OGD model, overexpression of miR-31 and silencing of PKD1 attenuated oxidative stress-induced neuronal injury, and diminished the lactate dehydrogenase leakage and reactive oxygen species level, accompanied by elevated neuronal viability. These results indicate that miR-31 alleviates inflammatory response as well as an oxidative stress-induced neuronal injury in IS mice by downregulating PKD1 and JAK/STAT3 pathway.