In the present study, a selenium-chondroitin sulfate (SeCS) was synthesized by the sodium selenite (Na2SeO3) and ascorbic acid (Vc) redox reaction using chondroitin sulfate derived from shark cartilage as a template, and characterized by SEM, SEM-EDS, FTIR and XRD. Meanwhile, its stability was investigated at different conditions of pH and temperatures. Besides, its antioxidant activity was further determined by the DPPH and ABTS assays. The results showed the SeCS with the smallest particle size of 131.3 ± 4.4 nm and selenium content of 33.18% was obtained under the optimal condition (CS concentration of 0.1 mg/mL, mass ratio of Na2SeO3 to Vc of 1:8, the reaction time of 3 h, and the reaction temperature of 25 °C). SEM image showed the SeCS was an individual and spherical nanostructure and its structure was evidenced by FTIR and XRD. Meanwhile, SeCS remained stable at an alkaline pH and possessed good storage stability at 4 °C for 28 days. The results on scavenging free radical levels showed that SeCS exhibited significantly higher antioxidant activity than SeNPs and CS, indicating that SeCS had a potential antioxidant effect.

The objective of the present study was to explore the protective effects of the curcumin/cyclodextrin polymer (CUR/CDP) inclusion complex on hydrogen peroxidecells damage. In this study, a H 2 O 2 -induced cells oxidative injury model was established to test the protective effects of the CUR/CDP inclusion complex. The cell viability of cells was detected by the thiazolyl blue tetrazolium bromide (MTT) assay. The extracellular lactate dehydrogenase (LDH) activity, catalase (CAT) activity, and malondialdehyde (MDA) level were detected by assay kits. The cellular reactive oxygen species (ROS) level was detected using the dichlorodihydrofluorescein (DCF) fluorescence assay. Western blotting analysis was conducted to assess the changes of phosphorylated-p53 and caspase-3. The results showed that 700 μM H 2 O 2 -treated LO2 cells for 3 h resulted in a significant decrease of cell viability to 53.00 ± 1.68%, which established the cell oxidative injury model. Cells treated with H 2 O 2 led to a significant increase of extracellular LDH activity, MDA content, and ROS level, and decreased CAT activity. Treatment with CUR/CDP significantly reversed the changes of the above indicators. Moreover, CUR/CDP treatment at 20 and 40 μg/ ml inhibited H 2 O 2 -induced increase in phosphorylated-p53 and caspase-3 expression, indicating that CUR/CDP suppressed cell apoptosis to alleviate liver injury. The results of those studies demonstrated that CUR/CDP had a protective effect on the oxidative damage of LO2 cells, and it could be developed as a new type of natural liver protection product to apply in the prevention of liver injury.

This study was to examine the protective effects of curcumin/cyclodextrin polymer inclusion complex (CUR/CDP) on ethanol‐induced liver injury in mice and to explore its potential mechanisms. In the ethanol‐induced acute injury mouse model, the effects of pretreatment with silymarin, cyclodextrin polymer (CDP), curcumin (CUR) and CUR/CDP at low, middle, and high doses were evaluated by biochemical and histopathological examination. The liver index, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) levels in serum of the mice were measured. The superoxide dismutase (SOD), glutathione peroxidase (GSH‐PX) activities, and malondialdehyde (MDA) level in liver tissue were assessed by assay kits. Moreover, hematoxylin–eosin (HE) staining was carried out to observe pathological changes of liver. Western blotting was performed for determining the changes in the expressions of DNA damage‐associated proteins. The results showed that compared with the control group, the liver index and the levels of ALT, AST, LDH, and MDA in the ethanol treatment group were significantly increased and the activities of GSH‐Px and SOD were obviously decreased. However, pretreatment with silymarin, CUR, and CUR/CDP reversed the change of above indicators except CDP. Moreover, CUR/CDP at high dose further weakened the liver index, inhibited the biochemical indexes, and enhanced the activities of antioxidant enzymes to a greater extent than silymarin and CUR. Western blot analysis indicated that CUR/CDP significantly down‐regulated the expressions of DNA damage‐related proteins including p‐ATM, γ‐H2AX, p‐p53, and p‐p38MAPK, which inhibited ethanol‐induced the G2/M arrest and ultimately prevented liver function from oxidative stress injury. These results indicated that CUR/CDP possessed good protective effect on mice liver damage in vivo by increasing the activities of GSH‐Px and SOD to suppress DNA damage.