Mango (Mangifera indica L.), a climacteric fruit of significant global economic value, suffers from rapid postharvest deterioration driven by complex hormonal and transcriptional networks. While chitosan coating is known to extend mango shelf-life, the precise molecular mechanisms, particularly its interplay with key ripening hormones like abscisic acid and ethylene, and the role of transcriptional regulators, remain poorly understood. We hypothesized that chitosan delays ripening by reprogramming abscisic acid and ethylene signaling pathways and associated transcriptional networks. To test this, we employed an integrative multi-omics approach combining transcriptomics and metabolomics to elucidate the molecular basis of chitosan-mediated ripening delay in mango fruit. Our findings reveal that chitosan orchestrates a dual hormonal attenuation associated with suppression of abscisic acid biosynthesis (NCED3, ABA2) and ethylene signaling (ETR1, EIN3/EIN4) while enhancing abscisic acid catabolism (CYP707A1/4). Crucially, γ-aminobutyric acid (GABA) accumulation antagonized abscisic acid to uncouple starch-to-sugar conversion from ripening progression, correlating with retained firmness and chlorophyll levels. Furthermore, we identified key transcription factors, WRKY53 and bZIP/RF2b, likely acts as central hubs modulating abscisic acid-ethylene crosstalk and cell wall integrity. This knowledge provides novel mechanistic insights into chitosan action and offers a foundation for developing targeted strategies to optimize postharvest preservation in climacteric fruits by synchronously modulating Abscisic acid-ethylene crosstalk, GABA-mediated metabolic reprogramming, and key TFs.

Although lychee peel extract (LPE) is rich in bioactive compounds, its potential for postharvest fruit preservation remains unexplored. We hypothesised that LPE would act synergistically with chitosan (CH) to delay mango ripening by simultaneously modulating cell wall integrity, pigment metabolism, and hormone signaling pathways. Here, we demonstrate that chitosan combined with lychee peel extract (CHL) delays mango ripening through a multi-targeted mechanism. Specifically, CHL outperformed chitosan alone by significantly suppressing peel yellowing, maintaining fruit firmness, and reducing decay over 12 days of storage. Integrated transcriptomic and metabolomic analyses revealed that LPE reprogrammed ripening-associated pathways by (1) upregulating cell wall remodeling genes (CSLE1, XTH23) to stabilize pectin architecture, (2) retaining chlorophyll via suppressed CRTISO and PSY (carotenoid synthesis) and enhanced CHLP (chlorophyll biosynthesis), and (3) decoupling sugar-acid dynamics through γ-aminobutyric acid (GABA) and succinic acid accumulation. Notably, LPE attenuated ethylene-auxin- abscisic acid (ABA) crosstalk by downregulating ripening-specific transcription factors (ERF003, bZIPs) while activating stress-responsive WRKYs. These findings establish LPE as a sustainable alternative to synthetic preservatives, leveraging agricultural byproducts for eco-friendly fruit preservation.

Chronic gastritis (CG) is linked to gut–gastric axis dysbiosis. Wenweishu Capsules (WWS) are clinically used to treat CG, but their concurrent regulatory effects on this axis remain unclear. A CG rat model was established using sodium deoxycholate, ammonia, ethanol, and irregular feeding. Rats received WWS (0.38 g·kg⁻¹·d⁻¹) for 4 weeks. Gastric lesions, inflammation, and gut microbiota were evaluated via histopathology, ELISA, 16S rRNA sequencing, PICRUSt prediction, and correlation analysis. WWS improved general condition, food intake, and weight gain in CG rats, alleviated gastric mucosal damage, and reduced serum TNF-α and IL-6. These effects were associated with altered IκBα expression and NF-κB pathway modulation. WWS reversed gut microbiota dysbiosis, restored α- and β-diversity, increased Lachnospiraceae NK4A136 group abundance, and suppressed potential pathogens. Functional prediction showed that WWS upregulated beneficial pathways such as carbohydrate metabolism and downregulated infection-related pathways. Correlation analysis linked TNF-α/IL-6 negatively with the Lachnospiraceae NK4A136 group and positively with Bacteroides. WWS ameliorates CG through a multi-dimensional mechanism that may involve modulation of the NF-κB inflammatory axis, rebalancing of gut microbiota structure, and remodeling of microbial metabolic function. These findings provide preliminary evidence for a potential microbe–drug interaction strategy for CG, though causal relationships require further mechanistic validation.