Abstract
Advanced glycation end products (AGEs) are harmful molecules formed through non-enzymatic reactions between proteins, lipids, and reducing sugars, contributing to diseases such as diabetes, Alzheimer’s, and cardiovascular conditions. This study investigates the inhibitory mechanisms of CMP-LSOPC nanoparticles (NPs) on AGEs release during gastrointestinal digestion. CMP-LSOPC NPs were synthesized by complexing carboxymethyl pachymaran (CMP) with lotus seedpod oligomeric procyanidins (LSOPC), its structure confirmed via FTIR, UV-Vis, SEM, and DSC analyses. In simulated gastrointestinal conditions, CMP-LSOPC NPs exhibited a significant reduction in AGE formation, achieving up to lowering AGE release by 48.5% compared to LSOPC alone. Furthermore, associated mechanisms are explored, including CMP-LSOPC NPs improving the stability, and antioxidant activity of LSOPC, inhibiting the activity of related hydrolase enzymes in the gastrointestinal environment. The CMP-LSOPC NPs group exhibited 4.1% higher LSOPC content during the gastric phase compared to LSOPC alone, indicating that CMP-LSOPC NPs having better stability. The antioxidant activity, measured through DPPH, ABTS+, and hydroxyl radical scavenging assays, demonstrated that CMP-LSOPC NPs enhanced antioxidant capacity, with a 35% increase in DPPH radical scavenging and 29% increase in ABTS+ radical scavenging compared to LSOPC alone. Enzyme inhibition assays showed a protective effect, with a 22% decrease in trypsin activity and 19% reduction in pepsin activity. Meanwhile, mass spectrometry revealed the presence of more long-chain glycopeptides in the CMP-LSOPC NPs group, which may exert beneficial influence on adiminishing the absorption of harmful AGEs. However, the potential risks of accumulating long glycated peptides in the colon should not be overlooked. Overall, CMP-LSOPC NPs effectively inhibited AGE release, which may offer a promising strategy for reducing dietary AGEs harm.
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