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Emodin (E), the main active ingredient in rhubarb, is a hydrophobic molecule. Micellar casein (MC) is the natural state of caseins in milk. In this study, the interaction between MC and E was calculated by fluorescence analysis with the addition of pectin (P). The average size and structure of P-MC@ E complexes were analyzed, as well as their DPPH free radical and ABTS cationic radical scavenging activities. In addition, the release profiles of emodin from the complexes were evaluated by a simulated gastrointestinal digestion experiment. Results showed that the major interaction between MC and emodin was hydrophobic forces in the P-MC system with the ratio of P to MC in the range of 0:10 - 5:5, the binding constant of which was greater than 103. With the increase of pectin content, the particle size of P-MC@ E complexes increased gradually, but its infrared spectra did not change significantly. Furthermore, the DPPH free radical and ABTS cationic radical scavenging activities of the complexes were significantly higher than those of free emodin, which increased with the increase of pectin content. After binding with P-MC, the release rate of emodin during simulated gastrointestinal digestion decreased. The results could provide basic references for the loading and delivery of emodin. [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the neuroprotective and antioxidant effects of Auxis thazard peptides (ATP) and to study the neuroprotective effect of ATP in the HT-22 cell injury model induced by corticosterone and glutamic acid. The protective effects of ATP on HT-22 injured cells were investigated based on cell morphology, cell viability, cell function, and biochemical indicators. Results showed that the cell viability of HT-22 cells induced by 0.9 mmol/L corticosterone and 15.0 mmol/L glutamic acid for 24 h was about 50% . Under these conditions, 10 μg/ mL, 20 μg/ mL, and 40 μg/ mL ATP could significantly inhibit the decline in HT-22 cell viability induced by corticosterone and glutamic acid, increase the concentrations of serotonin, acetylcholinesterase and choline, reduce acetylcholine activity, inhibit cell damage induced by corticosterone, and inhibit oxidative stress induced by glutamic acid. The activities of superoxide dismutase, glutathione enzyme, and glutathione peroxidase were increased, and the production of oxidation products malondialdehyde and reactive oxygen species was decreased. [ABSTRACT FROM AUTHOR]

Curcumin (Cur) is a flavonoid derived from Curcuma longa L. that has been shown to have a variety of biological activities, but some previous studies have described its non-negligible negative effects on female reproduction and embryo development. To further explore the toxic stress effect, this study investigated apoptosis and autophagy of healthy buffalo (Bubalus bubalis) derived granulosa cells (GCs) exposed to Cur and/or autophagy inhibitors. Results showed that Cur declined viability of GCs in a concentration-dependent manner. Apoptosis was observed in Cur-treated GCs from 3 h. Meanwhile, under Cur stress, autophagosomes accumulated in cells, and the expression levels of autophagy key proteins LC3 and Beclin 1 were up-regulated, suggesting that Cur could induce autophagy in GCs. Early autophagy inhibitor 3-methyladenine (3-MA) increased the apoptosis rate of Cur exposed GCs, but the autophagosome degradation inhibitor chloroquine (CQ) had no effect on the apoptosis rate. The network pharmacological and molecular docking analysis indicated that the perturbation of IKK/NF-κB might be the cause of Cur toxicity toward GCs. This study unveiled another side of Cur pharmacological effects that programmed cell death can be induced by Cur in GCs, suggesting that it should be prudent to use Cur as a clinical drug for its side effects on the female reproductive system. [ABSTRACT FROM AUTHOR]