Preparation and antibacterial activities of chitosan-gallic acid/polyvinyl alcohol blend film by LED-UV irradiation.

Active blend films from chitosan-gallic acid (CGA) and polyvinyl alcohol (PVA) were prepared via a simple mixing and casting method through the addition of citric acid as a plasticizer. The CGA/PVA blend films were characterized using Fourier transform infrared spectroscopy (FT-IR). The mechanical properties including tensile strength (TS) and elongation at break (%E), degree of solubility (S) and swelling behavior (DS), water vapor adsorption, and antimicrobial activities of the CGA/PVA blend films with and without LED (light emitting diode)-UV irradiation were also investigated. The CGA/PVA blend films exposed to UV irradiation exerted a higher TS (43.5MPa) and lower %E (50.40), S (0.38) and DS (2.73) compared to the CGA/PVA blend films (TS=41.7MPa, %E=55.40, S=0.42, and DS=3.16) not exposed LED-UV irradiation, indicating that the cross-linkage between CGA and PVA had been strengthened by LED-UV irradiation. However, the water vapor adsorption in the CGA/PVA blend films increased due to the changes of surface roughness and pore volume after LED-UV irradiation, and all values increased by increasing the CGA concentrations in the CGA/PVA blend films. The antimicrobial activities of the CGA/PVA blend films showed that the efficient concentration of CGA in the CGA/PVA blend films was over 1.0%. Taken together, the CGA/PVA blend films have potential for use as food packing materials.

Induction of Nrf2-mediated phase II detoxifying/antioxidant enzymes in vitro by chitosan-caffeic acid against hydrogen peroxide-induced hepatotoxicity through JNK/ERK pathway.

Chemical modification of chitosan is a promising method for the improvement of biological activity. In this study, chitosan-caffeic acid (CCA) was prepared and its in vitro hepatoprotective ability against hydrogen peroxide-induced hepatic damage in liver cells was evaluated. Treatment with CCA (50-400 µg/mL) did not show cytotoxicity and also significantly (p < 0.05) recovered cell viability against 650 µM hydrogen peroxide-induced hepatotoxicity. CCA treatment attenuated reactive oxygen species generation and lipid peroxidation in addition to increasing cellular glutathione level in cultured hepatocytes. To validate the underlying mechanism, antioxidant and phase II detoxifying enzyme expressions, which are mediated by NF-E2-related factor 2 (Nrf2) activation, were analyzed and CCA treatment was found to increase the expression of superoxide dismutase-1 (SOD-1), glutathione reductase (GR), heme oxygenase-1 (HO-1), and NAD(P)H:quinine oxidoreductase 1 (NQO1). CCA treatment resulted in increased Nrf2 nuclear translocation. The phosphorylation of extracellular regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) by CCA treatment contributed to Nrf2 activation. Pharmacological blockade of ERK, JNK, and p38 MAPK revealed that SP600125 (JNK inhibitor) and PD98059 (ERK inhibitor) treatment reduced Nrf2 translocation into the nucleus while SB203580 (p38 inhibitor) exhibited weak inhibition. Collectively, CCA protects liver cells against hydrogen peroxide-induced injury and this ability is attributed to the induction of antioxidants and phase II detoxifying enzymes that are mediated by Nrf2 translocation via JNK/ERK signaling.

Risks of borderline liver enzyme abnormalities to the incidence of impaired fasting glucose and diabetes mellitus: a 7 year follow up study of workers.

BACKGROUND: The aim of this study was to identify the relationships between borderline serum liver enzyme abnormalities and the incidence of impaired fasting glucose (IFG) and diabetes mellitus (DM) during a 7-year follow-up of workers, and to evaluate the quantitative level of risks. METHODS: A total of 749 workers in an electronics manufacturing company were divided into the normal fasting blood glucose (n = 633), IFG (n = 98), and DM (n = 18) groups, according to the results of their health checkup in 2006. Among 633 workers in the normal group, excluding 55 workers who were impossible to follow, incidence rate and relative risks of 578 workers to the IFG or DM in 2013 according to the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyltransferase (γ-GTP) were investigated. The liver enzyme levels were categorized as A (normal), B (borderline elevation), and R (definite elevation) following the standard of the National Health Insurance Service of Korea. RESULTS: The incidence rate of IFG or DM based on ALT level was 9.7 % for the A, 30.0 % for B, and 15.4 % for R. According to γ-GTP, the incidence rate was 9.8 % for A, 34.5 % for B, and 25.0 % for R. The relative risk(RR) to the incidence of IFG or DM depending on the level of ALT were 3.09 in B and 1.59 in R compared to A. According to γ-GTP, RR was 3.52 in B and 2.55 in R compared to A. AST level was not related to the incidence of IFG or DM. A multiple logistic regression analysis with the incidence of IFG or DM as a dependent variable resulted in an odds ratio of 2.664(1.214-5.849) for B level ALT, 3.685(1.405-9.667) for B level of γ-GTP even after adjustment for other variables such as age, sex, body mass index, AUDIT score, systolic blood pressure, and triglyceride. CONCLUSIONS: Even borderline elevations of ALT and γ-GTP, but not AST, increased the incidence and risk of IFG or DM after 7 years. Borderline elevation of ALT and γ-GTP was identified as an independent risk factor of IFG or DM.