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In this study, a composite wall material was prepared by blending whey protein isolate-D-xylose mixture and their Maillard reaction product with sodium alginate, which were then used for encapsulating proanthocyanidin to fabricate proanthocyanidin microcapsules. By characterizing the morphology, investigating stability, and assessing the in vitro antioxidant activity of different proanthocyanidin microcapsules, the advantages of microencapsulation of proanthocyanidin and the superiority of using Maillard reaction product as a wall material were elucidated. The results indicated that the microcapsules formed using the Maillard reaction product achieved an encapsulation efficiency of 98.60%±0.09%, with a proanthocyanidin content of 49.97±0.87 mg/g and a particle size of 1219.61±388.24 μm, exhibiting good granular morphology. Compared to microcapsules without the Maillard reaction, those formed with it demonstrated enhanced stability under conditions of 90 ℃, pH≤4, pH=10, and in gastric digestion fluid. Furthermore, when the proanthocyanidin concentration reached 30 μg/mL, the microcapsules formed with the Maillard reaction product exhibited stronger in vitro antioxidant activity. This study lays the groundwork for further development and utilization of proanthocyanidin microcapsules, offering new insights into the development and advancement of proanthocyanidin microcapsule food products.

Objective: To investigate the protective effects of flavonomaside on HT22 mouse hippocampal neuronal cells by inhibiting the inflammatory response induced by lipopolysaccharide (LPS) in mouse microglia (BV2) and elucidate the underlying mechanisms. Methods: BV2 cells were categorized into control (Con), LPS model (1 μg/mL), flavonomaside low, medium, and high dose groups (50, 100, 200 μmol/L respectively), TLR4 inhibitor group (TAK, 10 μmol/L), and TAK+flavonomaside group (10 μmol/L+200 μmol/L). Nitric oxide (NO), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) levels in supernatants and cell viability were quantified. Western blot assessed the protein levels of TLR4, Myd88, NF-κB p65, and phosphorylated NF-κB p65 in BV2 cells. The BV2 cell supernatant from each group acted as conditioned medium (CM) on HT22 cells to measure cell viability and observe morphological changes. Western blot also detected the protein levels of Bax, Bcl-2, cleaved Caspase-3, and Caspase-3 in HT22 cells. Results: No significant difference in BV2 cell viability was observed with varying flavonomaside concentrations compared to the Con group. The flavonomaside (200 μmol/L) group showed a significant reduction in NO, TNF-α, and IL-6 secretion compared to the LPS group (P

In this study, we explored the relationship between the platelet endothelial aggregation receptor 1 (PEAR1) polymorphisms, platelet reactivity, and clinical outcomes in patients with minor stroke or transient ischemic attack (TIA). Randomized controlled trial subgroups were assessed, wherein patients received dual antiplatelet therapy for at least 21 days. Platelet reactivity was measured at different time intervals. Genotypes were categorized as wild-type, mutant heterozygous, and mutant homozygous. Clinical outcomes were evaluated after 90 days. The rs12041331 polymorphism predominantly influenced adenosine diphosphate channel platelet activity, with the AA genotype displaying significantly lower residual platelet activity to the P2Y12 response unit (p < 0.01). This effect was more evident after 7 days of dual antiplatelet treatment (p = 0.016). Mutant A allele carriers had decreased rates of recurrent stroke and complex endpoint events but were more prone to bleeding (p = 0.015). The rs2768759 polymorphism majorly impacted arachidonic acid (AA) channel platelet activity, which was particularly noticeable in the C allele carriers. Our regression analysis demonstrated that rs12041331 AA + GA and rs2768759 CA predicted 90-day post-stroke bleeding. In conclusion, the PEAR1 polymorphisms rs12041331 and rs2768759 interfere with platelet aggregation and the performance of antiplatelet drugs. These genetic variations may contribute to bleeding events associated with minor stroke and TIA.