Molecular Nutrition & Food Research最新文献

This study investigated the protective effects of Lactobacillus plantarum NXU0014 against chronic alcoholic liver injury (CALI) and its underlying mechanisms in a mouse model. Forty-eight male C57BL/6J mice were divided into four groups: blank control, model, silymarin, and L. plantarum NXU0014. The CALI model was induced by administering 56% Hongxing Erguotou liquor. Multi-omics analyses revealed that alcohol intake induced gut microbiota dysbiosis, characterized by an increased Firmicutes/Bacteroidetes ratio and decreased abundance of probiotics (e.g., Lactobacillus and Bifidobacterium). These changes were associated with hepatic pro-inflammatory upregulation, downregulation of antioxidant genes (Nrf2, HO-1), and impaired intestinal barrier function (ZO-1). Metabolomic disturbances featured elevated fecal bile acids, reduced amino acids, and enriched pathways for ABC transporters and bile secretion. Intervention with NXU0014 restored probiotic levels (including Bifidobacterium pseudodanubicum and Lactobacillus reuteri), alleviated hepatic inflammation and oxidative stress by activating the Nrf2/HO-1 pathway, and repaired the intestinal barrier. Integrated microbiome-metabolome analysis revealed a negative correlation between Lactobacillus and toxic bile acids, and a positive correlation between Bifidobacterium and anti-inflammatory metabolites. These findings demonstrate that NXU0014 mitigates liver injury by modulating gut-liver axis metabolic interactions, highlighting its potential as a novel probiotic-based therapy for alcoholic liver disease.

Osteoarthritis (OA), a chronic degenerative joint disease, leads to disability and increases the health burden. This study identified the chemical components in the ethanol extract of propolis (EEP) and investigated its effects and mechanism on monosodium iodoacetate-induced OA in mice. Three phenolic acid esters, alongside 16 flavonoids and their derivatives, were tentatively characterized in EEP using HPLC–MS, and four main components were quantified. EEP treatment alleviated pathological changes in articular cartilage and reduced serum CTX-II levels in OA mice. Network pharmacology and molecular docking predicted that pro-inflammatory cytokines (e.g., TNF-α) and apoptosis-related factors (e.g., Bcl-2) could be key targets for propolis treatment of OA-related diseases. Subsequently, EEP decreased serum TNF-α, IL-1β, and IL-6 levels; increased the mRNA expression of Bcl-2; and reduced the mRNA expression of Caspase 8 and Bax in OA mice knee joints. Meanwhile, EEP decreased the mRNA expression of extracellular matrix-degrading enzymes in knee joints. Furthermore, through a combination of molecular docking, molecular dynamics simulations, RNA-seq, qRT–PCR, and Western blot assays, this study confirmed that EEP alleviated OA through regulating NF-κB and Hippo signaling pathways in the affected joints. These findings offer scientific evidence for the use of propolis in OA treatment.

Hypertensive nephropathy (HN), a significant consequence of chronic hypertension, remains a leading contributor to end-stage renal disease. Excessive Angiotensin II (Ang II)–driven inflammation, apoptosis, and fibrosis are central to its pathogenesis. Salvianolic acid A (SAA), a polyphenolic compound from Salvia miltiorrhiza, has anti-inflammatory properties, but its therapeutic potential in HN is unclear. HN was induced in mice by continuous subcutaneous infusion of Ang II (1.44 mg/kg/day) for 28 days. SAA (10 or 20 mg/kg/day) was administered orally every day during the final 14 days. Network pharmacology suggested SAA targets the TLR4/PI3K/AKT/NF-κB pathway. SAA administration improved renal function and attenuated inflammatory infiltration, tubular cell apoptosis, and interstitial fibrosis, independent of systemic blood pressure. NRK-52E cells were used in vitro. SAA inhibited PI3K and AKT phosphorylation, suppressed NF-κB P65 activation, and downregulated pro-inflammatory cytokines. The PI3K activator 740 Y-P abolished these effects. Pull-down, DARTS assays and molecular docking showed interaction between SAA and TLR4, while TLR4 overexpression reversed SAA's protective actions. These findings provide the evidence that SAA exerts protective effects against Ang II-induced HN, acting through inhibition of the TLR4/MyD88/PI3K/AKT/NF-κB axis and represents a potential TLR4-targeted therapy for hypertensive kidney injury.

Photoaging of the skin, driven by ultraviolet B (UVB) radiation, is characterized by the upregulation of matrix metalloproteinases (MMPs), accelerated collagen degradation, diminished hyaluronic acid (HA) content, and disruption of extracellular matrix (ECM) integrity, culminating in wrinkle formation, and structural damage. Nutritional and plant-derived compounds have garnered increasing attention as promising therapeutic agents for skin aging. In this study, we explored the anti-photoaging effects of Gynostemma pentaphyllum hydrodistillate (GPHD) and its bioactive constituent, Damulin B, in UVB-irradiated in vivo and in vitro models. In HR-1 hairless mice, GPHD treatment significantly ameliorated UVB-induced wrinkle formation, collagen degradation, epidermal hyperplasia, and transepidermal water loss, while improving hydration and elasticity. It also modulated hyaluronic acid metabolism by upregulating hyaluronic acid synthases (HAS1 and HAS2) and downregulating hyaluronidases (HYAL1 and HYAL2). In UVB-irradiated Hs68 fibroblasts, GPHD and Damulin B attenuated reactive oxygen species (ROS) generation, thereby inhibiting mitogen-activated protein kinase/activator protein-1 (MAPK/AP-1) signaling and restoring transforming growth factor-beta/Smad (TGF-β/Smad) activity, ultimately contributing to ECM stability. Collectively, our findings demonstrate that GPHD and Damulin B exert potent anti-photoaging effects by mitigating oxidative stress and orchestrating downstream signaling pathways essential for ECM remodeling and skin homeostasis.

Chronic obstructive pulmonary disease (COPD) is primarily induced by chronic cigarette smoke (CS) exposure, which triggers irreversible airway inflammation and remodeling. Although Canarium album L. (CA) has been historically utilized to alleviate respiratory symptoms, its efficacy and mechanisms against COPD remain poorly characterized. This study aimed to investigate the anti-COPD potential of CA and further explore its crucial bioactive constituents. In this work, the phytochemicals and 15 phenolic compounds of eight varieties of CA were determined. Network pharmacology was used to search COPD targets and related pathways. The active constituents were screened, and the efficacy and mechanism of CA against COPD were uncovered based on the CS-induced Beas-2B cell model combined with spectrum-effect analyses and molecular docking. The results suggested that CA could reduce the release of inflammatory mediators and the expressions of COX-2 and iNOS via downregulating MAPK signaling pathway to mitigate COPD. Among them, (+)-catechin, epicatechin and (−)-epigallocatechin showed stronger correlations and better interactions with the core targets of COPD, they might be the effective components. This study lays foundation for understanding the potential of CA in COPD treatment and provides guidance for subsequent functional food development.