Effect of H2O2-assisted ultrasonic bath on the degradation and physicochemical properties of pectin.

The effects of H2O2-assisted ultrasonic bath degradation technology on pectin were investigated. The degradation efficiency with different pectin concentrations, H2O2 concentrations, ultrasonic power, and ultrasonic time was analyzed. The results showed that pectin concentration was negatively correlated with the degradation efficiency of pectin, while, H2O2 concentration, ultrasonic power, and ultrasonic time were positive correlated with the degradation efficiency. Besides, the apparent viscosity and viscoelasticity of the degraded pectin decreased significantly. The antioxidant activity increased after the H2O2-assisted ultrasonic bath treatment. The results of FTIR, NMR, laser particle size, SEM, XRD, and AFM analysis indicated that the degradation treatment did not destroy the main structure of pectin. The average particle size and crystallinity of pectin decreased. The degree of aggregation and the height of the molecular chain decreased significantly. In conclusion, the H2O2-assisted ultrasonic bath degradation technique could effectively degrade pectin. This study provided a comprehensive analysis of the degradation of pectin under H2O2-assisted ultrasonic bath, which will be beneficial to further develop H2O2-assisted ultrasonic bath techniques for pectin degradation.

Schisantherin A alleviated alcohol-induced liver injury by the regulation of alcohol metabolism and NF-kB pathway.

Schisantherin A (SinA), one of the most abundant active ingredients of Schisandra chinensis, was reported to protect and benefit the liver, however, its effect on alcohol-induced liver injury (ALI) was still not clear. In the present study, an ALI mice model was induced by feeding mice an alcohol-containing liquid diet for four weeks. Then, 100 mg/kg or 200 mg/kg SinA was administered to mice every day by gavage for the last two weeks. Histopathological analysis showed that alcohol-induced liver lipid vacuoles were reduced by SinA. The activities of aspartate aminotransferase (AST, 61.90 ± 14.65 vs. 93.65 ± 20.50, 50.46 ± 13.21 vs. 93.65 ± 20.50) and alanine transaminase (ALT, 41.29 ± 9.20 vs. 64.04 ± 18.13, 36.52 ± 7.71 vs. 64.04 ± 18.13) in the serum of ALI mice were significantly reduced by 100 mg/kg or 200 mg/kg SinA when compared with control mice. Alcohol-induced oxidative stress and the inflammatory response in the liver were suppressed by SinA in a dose-dependent manner. Meanwhile, treatment with SinA decreased alcohol dehydrogenase (ADH) activity and increased acetaldehyde dehydrogenase (ALDH) activity in ALI mice. Alcohol-induced upregulation of CYP2E1 and CYP1A2 in the liver was inhibited by SinA. Further, SinA suppressed activation of the NF-kB pathway in ALI mice. In conclusion, our findings demonstrate that SinA is able to protect against ALI, and this may be, at least in part, caused by regulation of alcohol metabolism and the NF-kB pathway. Our data suggest a therapeutic potential of SinA in the treatment of ALI.