Effects of ginger essential oil on physicochemical and structural properties of agar­sodium alginate bilayer film and its application to beef refrigeration.

To maintain the freshness of meat products, an agar­sodium alginate (AS) bilayer antibacterial film incorporated with ginger essential oil (GEO) was developed. The effect of GEO at different concentrations (1%, 2%, 3% and 4% v/v) on the physical properties, micro-structure and antibacterial activity closely related to AS film's application to beef refrigeration was extensively studied. In addition, the effects of AS bilayer active film on refrigeration quality and shelf life of beef were systematically evaluated. The porous structure and number of oil droplets became more obvious with the increase of GEO amount in AS film. The incorporation and increase of GEO could delay the lipid oxidation and protein decomposition of beef, reduce the total counts of the tested microorganisms (total viable bacteria, psychrotrophic bacteria, Escherichia coli, Staphylococcus aureus, yeast, and mold) in meat samples. Compared with commercial polyethylene (PE) packaging, the accumulation of basic compounds from the degradation of beef protein as well as the microbial contamination was obviously improved, which could extend the comprehensive shelf life of beef by 4-6 days. Consequently, AS bilayer films incorporated with GEO, especially GEO at 4.0% (v/v) GEO concentration can be developed to be an antibacterial active packaging material for beef refrigeration.

PXDN reduces autophagic flux in insulin-resistant cardiomyocytes via modulating FoxO1.

Autophagy, a well-observed intracellular lysosomal degradation process, is particularly important to the cell viability in diabetic cardiomyopathy (DCM). Peroxidasin (PXDN) is a heme-containing peroxidase that augments oxidative stress and plays an essential role in cardiovascular diseases, while whether PXDN contributes to the pathogenesis of DCM remains unknown. Here we reported the suppression of cell viability and autophagic flux, as shown by autophagosomes accumulation and increased expression level of LC3-II and p62 in cultured H9C2 and human AC16 cells that treated with 400 µM palmitate acid (PA) for 24 h. Simultaneously, PXDN protein level increased. Moreover, cell death, autophagosomes accumulation as well as increased p62 expression were suppressed by PXDN silence. In addition, knockdown of PXDN reversed PA-induced downregulated forkhead box-1 (FoxO1) and reduced FoxO1 phosphorylation, whereas did not affect AKT phosphorylation. Not consistent with the effects of si-PXDN, double-silence of PXDN and FoxO1 significantly increased cell death, suppressed autophagic flux and declined the level of FoxO1 and PXDN, while the expression of LC3-II was unchanged under PA stimulation. Furthermore, inhibition of FoxO1 in PA-untreated cells induced cell death, inhibited autophagic flux, and inhibited FoxO1 and PXDN expression. Thus, we come to conclusion that PXDN plays a key role in PA-induced cell death by impairing autophagic flux through inhibiting FoxO1, and FoxO1 may also affect the expression of PXDN. These findings may develop better understanding of potential mechanisms regarding autophagy in insulin-resistant cardiomyocytes.