Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by Aβ deposition, tau hyperphosphorylation, and neuroinflammation. No effective drugs can slow disease progression. Polysaccharides from traditional Chinese medicine (TCM) exhibit neuroprotective activities (e.g., antioxidant, anti-inflammatory) with good safety. However, their clinical application is limited by low oral bioavailability, poor blood–brain barrier (BBB) permeability, and a pharmacokinetic–pharmacodynamic paradox. The emerging role of the microbiota–gut–brain axis in AD offers a strategy to overcome this paradox. This review summarizes the structural features and classification of TCM polysaccharides (from plants, fungi, and roots/rhizomes) and highlights their anti-AD mechanisms via the gut–brain axis. Acting as prebiotics, these polysaccharides escape upper digestion and are fermented by gut microbiota into short-chain fatty acids (SCFAs) and other metabolites, which enter circulation, cross the BBB, and alleviate AD pathology through metabolic, immune, and neuronal pathways. Outcomes include reduced Aβ deposition and tau phosphorylation, suppressed neuroinflammation, restored synaptic function, and improved cognition. This review provides a theoretical framework for TCM polysaccharide intervention in AD via the gut–brain axis and a pharmacological basis for developing natural product-based AD therapies.
Jie Gao, Liheng Li, Qi Liu et al.· Molecules· 0 citations
BACKGROUND
Prenatal exposure to parabens (PBs) has been associated with infantile eczema; however, the mediating role of inflammatory cytokines and the potential modifying effect of breastfeeding remain unclear.
METHODS
This prospective study included 336 mother-infant dyads. Maternal serum concentrations of five parabens, namely methylparaben (MeP), ethylparaben (EtP), propylparaben (PrP), butylparaben (BuP), and hexylparaben (HeP), and eight inflammatory cytokines were measured during pregnancy. Infantile eczema and feeding patterns during the first six months were recorded. Weighted quantile sum (WQS) regression assessed mixture effects; single-chemical associations were examined using covariate-adjusted logistic and linear regression. Mediation and moderated mediation analyses were performed to evaluate the role of interleukin-17A (IL-17A) and the modifying effect of breastfeeding. Network toxicology was employed to identify shared molecular targets and pathways.
RESULTS
The PBs mixture was significantly associated with increased eczema risk (WQS OR = 1.97, 95% CI: 1.24-3.12). In single-chemical models, PrP (OR = 1.08, 95% CI: 1.02-1.15) and HeP (OR = 1.38, 95% CI: 1.02-1.87) were positively associated with eczema. Maternal PrP was positively associated with serum IL-17A (β = 0.034, 95% CI: 0.006-0.063). Elevated IL-17A was strongly associated with eczema (OR = 3.46, 95% CI: 1.45-8.26). IL-17A accounted for approximately 14.9% of the association between PrP and eczema (indirect effect β = 0.003, 95% CI: 0.001-0.010). Moderated mediation revealed that breastfeeding significantly modified the pathway from IL-17A to eczema (interaction P = 0.018). The indirect effect was significant only in formula-fed infants (β = 0.069, P = 0.040) and absent in breastfed infants (P = 0.680). Network toxicology identified 11 common targets of PrP and eczema enriched in IL-17, Toll-like receptor, and NF-κB signaling pathways.
CONCLUSIONS
Maternal IL-17A may partially mediate the association between prenatal PrP exposure and infantile eczema, and breastfeeding may modify the association between IL-17A and eczema. These findings support the importance of further evaluating prenatal paraben exposure during pregnancy and promoting breastfeeding to mitigate early-life allergic disease risk.
M. Chang, Xian-Jia Li, Ye Li et al.· Environmental Pollution· 0 citations
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