Central blockage of sympathetic nerves inhibits the abnormal vital signs and disturbance of the gut microbiota caused by continuous light exposure.

Background: Continuous light exposure increases sympathetic excitation in rats, leading to hypertension, left ventricular hypertrophy, and fibrosis. This study was aimed to investigate whether continuous light exposure causes destabilization of vital signs and gut microbiota (GM) in Sprague Dawley (SD) rats and whether clonidine hydrochloride (CH), a central sympathetic depressant drug, could prevent these changes. Methods: Eight-week-old male SD rats were divided into three groups with different interventions for 14 weeks: control group (CG), 2-mL pure water gavaged daily while on a normal 12-h light/dark cycle; continuous illumination group (CI), 2-mL pure water gavaged daily while receiving continuous exposure to light (300 lx); and drug administration group (DA), CH (10 µg/kg) gavaged daily while receiving continuous exposure to light (300 lx). Results: The results showed that blood pressure, heart rate, and body weight were significantly higher in the CI group than in the CG and DA groups (P < 0.05). Moreover, the Shannon index was higher in the DA group than in the CI group (P = 0.012). The beta diversity index in the CG group was significantly higher in the CI group (P = 0.039). The pairwise comparison results of the linear discriminant analysis effect size showed that Oscillospirales were enriched in the DA group, whereas the Prevotellaceae lineage (family level) > Prevotella (genus level) > Prevotellaceae_bacterium (species level) were enriched in the CI group. The Muribaculaceae family was more abundant in the CG group than in the CI group. Conclusion: Sympathetic nerve inhibition restored the abnormal vital signs and GM changes under continuous light exposure.

Novel amphiphilic polymeric ionic liquid-solid phase micro-extraction membrane for the preconcentration of aniline as degradation product of azo dye Orange G under sonication by liquid chromatography-tandem mass spectrometry.

A novel amphiphilic polymeric ionic liquid membrane containing a hydrophilic bromide anion and a hydrophobic carbonyl group was synthesized in dimethylformamide (DMF) systems using the ionic liquid 1-butyl-3-vinylimidazolium bromide (BVImBr) and the methylmethacrylate (MMA) as monomers. The prepared amphiphilic ploy-methylmethacrylate-1-butyl-3-vinylimidazolium bromide (MMA-BVImBr) was characterized by a scanning electron microscope and an infrared spectrum instrument. The results of solid-phase micro-extraction membrane (SPMM) experiments showed that the adsorption capacity of membrane was about 0.76µgµg(-1) for aniline. Based on this, a sensitive method for the determination of trace aniline, as a degradation product of azo dye Orange G under sonication, was developed by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The calibration curve showed a good linearity ranging from 0.5 to 10.0µgL(-1) with a correlation coefficient value of 0.9998. The limit of quantification was 0.5µgL(-1). The recoveries ranged from 90.6% to 96.1%. The intra- and inter-day relative standard deviations were less than 8.3% and 10.9%. The developed SPMM-LC-MS/MS method was used successfully for preconcentration of trace aniline produced during the sonication of Orange G solution.

[Effects of FOXP3 on the progression of atherosclerosis plaque in ApoE-knock out mice].

AIM: To explore effects of FOXP3 on the progression of atherosclerosis plaque in hypercholesterolemic apoliprotein(apo)E-/- mice. METHODS: At 8 weeks of age, 32 male ApoE-/- mice were randomly divided into four groups of eight. Labeled: negative control group, positive control group, small interfering RNA (siRNA) group, and regulatory T cells transfer (Tregs) group. Lentivirus-mediated (siRNA) identified its function by Western blot was used to knock down FOXP3 and Foxp3(high+);CD4(+); CD25(+); Tregs acquired through magnetic activated cell sorting adoptive transfer assays in high fat diet ApoE-/- mice were done. The resulting atherosclerotic lesions were assessed by determining the number and function of CD4(+);CD25(+); Tregs, FOXP3 transcript levels and investigating the expression of Foxp3 protein in different tissues. Inflammatory cytokines were determined by ELISA. RESULTS: Animals treated with siRNA of FOXP3 showed a significant increase in atherosclerotic lesion formation and a reduction in the number and function of Foxp3(+);CD4(+);CD25(+); Tregs compared with other groups. Transfer of Foxp3(high+);CD4(+);CD25(+); Tregs significantly decreased atherosclerotic plaque formation and increased the number and function of Foxp3(+); CD4(+); CD25(+); Tregs. Foxp3 protein levels and FOXP3 transcript levels were lowest in the siRNA group, and were highest in tissues from the Tregs transfer group. CONCLUSION: FOXP3 plays an important role in regulating the inflammatory response within the atherosclerotic lesion. It can inhibit significant the progression of the atherosclerosis plaque in ApoE-/- mice.