Effect of Lactobacillus plantarum enriched with organic/inorganic selenium on the quality and microbial communities of fermented pickles.

Lactobacillus enriched with organic/inorganic selenium and pickles fermented with the Lactobacillus plantarum R were prepared. The results showed that selenium-enriched Lactobacillus plantarum R enhanced the antioxidant capacity, inhibition rate of advanced glycation end-products (AGEs), nitrite degradation, and the organic acid production of fermented pickles, while Lactobacillus plantarum R enriched with inorganic selenium (R-Se-IN) showed the best performance. Twenty-three aroma-active substances and seven characteristic compounds were detected in the R-Se-IN group. Moreover, the bacterial community result revealed that Lactococcus, Lactobacillus, and Leuconostoc were predominant in the R-Se-IN group, while the other groups contained Enterobacter, Halomonas, and Klebsiella. Furthermore, the correlations between environmental factors, differential flavor substances, and microbial communities were explored based on multivariate statistical analysis. These results indicate that the addition of Lactobacillus plantarum R enriched with organic/inorganic selenium influenced the environmental factors, differential flavor substances, and microbial communities of the fermented pickles.

Knockdown of lncRNA TUG1 attenuates cerebral ischemia/reperfusion injury through regulating miR-142-3p.

Cerebral ischemia-reperfusion injury (CI/RI) is one of the most common diseases of the central nervous system. At present, there is no specific treatment for CI/RI. It is necessary to explore the mechanism of CI/RI and find new ways to prevent and treat CI/RI. An oxygen and glucose deprivation/recovery (OGD/R) model was established to evaluate the effects of mouse astrocytes (MA-C) cell viability and apoptosis of stepwise exposure to oxygen and glucose deprivation followed by their replenishment. This assessment included using taurine upregulated gene 1-small interfering RNAs (TUG1-siRNA) transfection to determine the effects of TUG1 knockdown on MA-C survival and apoptosis. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to evaluate TUG1 and miR-142-3p expression levels. The luciferase gene reporter assay was performed to validate that miR-142-3p is a TUG1 target. Accordingly, the effects of miR-142-3p knockdown on TUG1-induced MA-C apoptosis were determined using flow cytometry. Methyl thiazolyl tetrazolium (MTT) method was used to detect cell growth viability. Western blotting analysis was performed to detect the expression levels of apoptosis-related proteins. TUG1 was upregulated, while miR-142-3p was downregulated in the OGD/R model of MA-C cells. Inhibiting the expression of TUG1 could protect MA-C cells and reverse the decrease in growth viability and increasing apoptosis of MA-C cells caused by OGD/R stimulation. On the other hand, the inhibition of miR-142-3p offset the effect of TUG1 knockdown on cell viability and apoptosis. Inhibition of OGD/R-induced increases in TUG1 expression that in turn reduces miR-142-3p upregulation may suppress reperfusion-induced losses in cell viability.