Pengjie Wang

The development of thermally stable Type 5 resistant starch (RS5) is critical for functional food applications to modulate glycemic responses. This study investigated the structural assembly and enzymatic resistance of RS5 complexes prepared from high-amylose maize starch (HAMS) via a sequential strategy coupling pullulanase debranching with heat–moisture treatment (HMT). HAMS was debranched for varying durations (0–24 h) to generate short, linear glucan chains, subsequently complexed with myristic acid (MA) or linoleic acid (LOA), and further modified by pressure–heat treatment (PHT) or annealing (ANN). Extended debranching (24 h) significantly enhanced the complexing index and resistant starch (RS) content. While saturated MA promoted higher crystallinity of the hexagonal Bravais lattice, unsaturated LOA effectively enhanced resistance through steric hindrance despite lower crystallinity. Notably, PHT generally outperformed ANN, with the highest RS content (69.2%) achieved in DH24-LOA complexes treated at 120 °C with 10% moisture. Multi-scale structural analyses revealed that resistance originated from the transition of amorphous chains into highly ordered, thermally stable nanocrystals possessing a hexagonal Bravais lattice and the densification of the macroscopic architecture. These findings demonstrate that coupling pullulanase debranching with optimized PHT is a potent strategy to engineer high-performance RS5 ingredients with superior digestive resistance.

Background/Objectives: Hippocampal neuroinflammation (HNF) is a key pathological feature in neurodegenerative disorders. Milk-derived exosomes, as bioactive extracellular vesicles, have underexplored potential in regulating brain neuroinflammatory responses. This study aimed to characterize desert milk exosomes (D-Exo) and investigate their neuroprotective and anti-neuroinflammatory effects in LPS-induced HNF mice model and an LPS-stimulated BV2 microglia. Methods: Exosomes were isolated from desert and non-desert milk (ND-Exo) for proteomic analysis. After pretreating BV2 cells with exosomes and stimulating with LPS, their inflammatory responses and polarization were assessed by RT-PCR. Balb/c mice were orally gavaged with D-Exo or 0.9% NaCl for 28 days before LPS injection. Cognitive function was assessed via behavioral tests, with microglial/astrocyte activation analyzed by immunofluorescence. Results: D-Exo exhibited superior stability and a unique proteomic profile enriched with proteins linked to neuroinflammation and blood-brain barrier (BBB) integrity, notably within the AMPK signaling pathway. In vitro, D-Exo shifted LPS-stimulated microglia from the M1 to the M2 phenotype. In vivo, it alleviated HNF and cognitive decline, reduced Aβ_1-42 and Tau deposition, elevated BDNF and MAP2, and suppressed neuroinflammation and glial activation. Conclusions: D-Exo is enriched with specific proteins, attenuates neuroinflammation and cognitive decline by regulating microglial M1/M2 polarization and AMPK pathway, highlighting its preventive potential.