Coenzyme Q10 Protects Astrocytes from Ultraviolet B-Induced Damage Through Inhibition of ERK 1/2 Pathway Overexpression.

Overexpression of extracellular signal-regulated kinase ½ (ERK ½) signaling pathway leads to overproduction of reactive oxygen species (ROS) which induces oxidative stress. Coenzyme Q10 (CoQ10) scavenges ROS and protects cells against oxidative stress. The present study was designed to examine whether the protection of Coenzyme Q10 against oxidative damage in astrocytes is through regulating ERK 1/2 pathway. Ultraviolet B (UVB) irradiation was chosen as a tool to induce oxidative stress. Murine astrocytes were treated with 10 µg/ml and 25 µg/ml of CoQ10 for 24 h prior to UVB and maintained during UVB and 24 h post-UVB. Cell viability was evaluated by counting viable cells and MTT conversion assay. ROS production was measured using fluorescent probes. Levels of p-ERK 1/2, ERK 1/2, p-PKA, PKA were detected using immunocytochemistry and/or Western blotting. The results showed that UVB irradiation decreased the number of viable cells. This damaging effect was associated with accumulation of ROS and elevations of p-ERK 1/2 and p-PKA. Treatment with CoQ10 at 25 µg/ml significantly increased the number of viable cells and prevented the UVB-induced increases of ROS, p-ERK 1/2, and p-PKA. It is concluded that suppression of the PKA-ERK 1/2 signaling pathway may be one of the important mechanisms by which CoQ10 protects astrocytes from UVB-induced oxidative damage.

Low-power total internal reflection thermo-optic switch based on hybrid SiON-polymer X-junction waveguides.

We propose and demonstrate a low-power 2×2 total internal reflection thermo-optic switch based on an X-junction configuration formed with a silicon oxynitride (SiON) core and polymer cladding. Unlike X-junctions reported thus far, our proposed configuration features a slot formed on the center of the X-junction and filled with polymer cladding. With such a configuration, the opposite thermo-optic characteristics of SiON and polymer and, hence, heat utilization efficiency can be fully utilized. Our fabricated proof-of-principle switch shows extinction ratios of larger than 15.34 dB and switching powers of less than ∼59.6 mW. The rise time and fall time of switching are 1.42 and 0.85 ms, respectively. The insertion losses are less than 10.6 dB for all channels, and the polarization-dependent loss is ∼0.3 dB.

Liver Metabolomics Reveals the Effect of Lactobacillus reuteri on Alcoholic Liver Disease.

Alcoholic liver disease (ALD), a type of chronic liver disease that is prevalent worldwide, is still identified to have a poor prognosis despite many medical treatment protocols. Thus, it is urgent to develop and test new treatment protocols for ALD. Lactobacillus reuteri (L. reuteri) has been widely used in the clinical treatment of digestive system diseases, but studies on the protective effect of L. reuteri on ALD are considered to be rare. Therefore, in the present study, we examined the effect of L. reuteri on ALD and provide data that are significant in the development of new treatment protocols for ALD. An ALD model has been established in C57BL/6J mice treated according to the Gao-binge modeling method. Mice in the treatment group were administered with L. reuteri. Hematoxylin and eosin (H&E) staining, oil red O staining, immunohistochemistry, and biochemical analyses were performed to detect the phenotypic changes in the liver among mice in the different treatment groups. L. reuteri treatment reversed inflammatory cell infiltration and lipid accumulation. Moreover, AST, ALT, TG, and TCH levels were also reduced in the probiotics-treatment group. Five candidate biomarkers were found in the liver metabolites of different treatment groups by UPLC/QTOF-MS and a multivariate analysis. Several fatty acid metabolic pathways such as linoleic acid metabolism and glycerolipid metabolism were involved. All these findings suggested that L. reuteri treatment reversed the phenotype of ethanol-induced hepatitis and metabolic disorders. These findings provide evidence that L. reuteri might serve as a new therapeutic strategy for ALD.