Formation mechanism of quinoa protein hydrolysate-EGCG complexes at different pH conditions and its effect on the protein hydrolysate-lipid co-oxidation in emulsions.

This study aimed to investigate the interaction, structure, antioxidant, and emulsification properties of quinoa protein hydrolysate (QPH) complexes formed with (-)-epigallocatechin gallate (EGCG) at pH 3.0 and 7.0. Additionally, the effect of pH conditions and EGCG complexation on protein hydrolysate-lipid co-oxidation in QPH emulsions was explored. The results indicated that QPH primarily interacted with EGCG through hydrophobic interactions and hydrogen bonds. This interaction led to alterations in the secondary structure of QPH, as well as a decrease in surface hydrophobicity and free SH content. Notably, the binding affinity between QPH and EGCG was observed to be higher at pH 7.0 compared to pH 3.0. Consequently, QPH-EGCG complexes exhibited more significant enhancement in antioxidant and emulsification properties at pH 7.0 than pH 3.0. The pH level also influenced the droplet size, ζ-potential, and interfacial composition of emulsions formed by QPH and QPH-EGCG complexes. Compared to QPH stabilized emulsions, QPH-EGCG stabilized emulsions were more capable of mitigating destabilization during storage and displayed fewer lipid oxidation products, carbonyl generation, and sulfhydryl groups and fluorescence loss, which implied better oxidative stability of the emulsions. Furthermore, the QPH-EGCG complexes formed at pH 7.0 exhibited better inhibition of protein hydrolysate-lipid co-oxidation. Overall, these findings provide valuable insights into the potential application of QPH and its complexes with EGCG in food processing systems.

Development of Novel Nanocarriers by Ultrasound and Ethanol-Assisted Soy Protein Isolate: Enhancing the Resistance of Lutein to Environmental Stress.

The aim of this work was to investigate the effects of the processing sequence of ultrasound and ethanol on the physicochemical properties of soy protein isolate (SPI), which were further evaluated for the morphology and stability of SPI-lutein coassembled nanoparticles. The results showed that the sequence of ultrasound followed by ethanol treatment was the optimal one. The samples were subjected to ultrasonication followed by subunit disassembly and reassembly induced by 40% (v/v) ethanol, with the resulting molecular unfolding and subsequent aggregation being attributed to intramolecular hydrogen bonds. The recombined nanoparticles had smaller particle size (142.43 ± 2.91 nm) and turbidity (0.16 ± 0.01), and the exposure of more hydrophobic groups (H0 = 6221.00 ± 130.20) induced a shift of SPI structure toward a more ordered direction. The homogeneous and stable particle provided excellent stability for the loading of lutein. The bioaccessibility (from 25.48 ± 2.35 to 65.85 ± 1.78%) and release rate of lutein were modulated in gastrointestinal digestion experiments. Our discoveries provide a new perspective for the development of combined physicochemical modification of proteins as nanocarriers in functional foods.

Lipoxin A4 methyl ester ameliorates cognitive deficits induced by chronic cerebral hypoperfusion through activating ERK/Nrf2 signaling pathway in rats.

Lipoxin A4 (LXA4) is known for its powerful anti-inflammatory function. Current studies in vitro suggest that LXA4 possesses novel antioxidant effect. The aim of this study is to examine whether Lipoxin A4 methyl ester (LXA4 ME) has neuroprotective effects against chronic cerebral hypoperfusion, and if so, whether the effects of LXA4 ME are associated with its potential antioxidant property. Adult male Sprague-Dawley rats were subjected to permanent bilateral common carotid artery occlusion (BCCAO) and randomly assigned into four groups: sham (sham-operated) group, vehicle (BCCAO+normal saline) group, LXA4 ME10 (BCCAO+LXA4 ME 10 ng per day) group and LXA4 ME100 (BCCAO+LXA4 ME 100 ng per day) group. LXA4 ME was administered through intracerebroventricular injection for 2 consecutive weeks. LXA4 ME significantly alleviated spatial learning and memory impairments, as assessed by Morris water maze and inhibited the loss of neurons in the CA1 region of the hippocampus. Biochemically, LXA4 ME phosphorylated extracellular signal regulated kinase (ERK) 1/2 and enhanced nuclear factor erythroid 2-related factor 2 (Nrf2) expression and its nuclear translocation, as well as NAD(P)H: quinone oxidoreductase 1 (NQO1) expression. LXA4 ME reduced lipid peroxidative production in the hippocampus, as measured by immunohistochemical staining for 4-Hydroxynonenal (4-HNE). In addition, LXA4 ME significantly elevated the ratio of Bcl-2/Bax and decreased cleaved caspase-3 expression in the hippocampus. Therefore, these data suggest that LXA4 ME exerts beneficial effects on the cognitive impairment induced by chronic cerebral hypoperfusion through attenuating oxidative injury and reducing neuronal apoptosis in the hippocampus, which is most likely associated with the activation of ERK/Nrf2 signaling pathway.

Protective effect of donepezil hydrochloride on cerebral ischemia/reperfusion injury in mice.

The aim of this study was to investigate the effects of donepezil hydrochloride (DH) on the expression of the calpain I-cyclin-dependent kinase5/p25 (CDK5/p25) pathway in the hippocampal CA1 region in mice with cerebral ischemia-reperfusion (I/R). Mice were randomly divided and assigned to the sham operation group (SO), the model group (MG) and the DH treatment group (TG). The pathological appearance of the hippocampal CA1 region and the expression of calpain I and CDK5/p25, were observed on the 4th, 6th and 8th week of the I/R surgery. Within the same time periods, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were also determined. At each postoperative time point, the normal neuron count in the hippocampal CA1 region in the MG was significantly lower than that in the SO (P<0.05), whereas the calpain I and CDK5/p25 expression, SOD activity and MDA content in the MG were significantly higher than those in the SO (P<0.05). The normal neuron count of the hippocampal CA1 region in the TG increased significantly (P<0.05), whereas the calpain I and CDK5/p25 expression, SOD activity and MDA content in the TG were significantly lower than those in the MG (P<0.05). DH has protective effects against ischemic damage. The ability of DH to improve learning and memory in mice may be due to its ability to decrease the expression of the calpain I-CDK5/p25 pathway and reduce oxidative damage.