‘Huangguan’ pear (Pyrus bretschneideri Rehd. cv. Huangguan) fruit is sensitive to chilling injury (CI), which exhibits peel browning spots (PBS) during cold storage. Dehydrin (DHN) is considered to be related to cold tolerance in plants, but its function in postharvest pear fruit during storage remains unclear. In this study, six PbDHNs (PbDHN1–6) genes were identified and characterized, and the PbDHN proteins were sorted into Y_nK_n, SK_n and Y_nSK_n according to the major conserved motifs related to the number and location of K-segments, S-segments, and Y-segments. In addition, there were five cold-responsive related cis-acting elements in the promoter region of the PbDHNs. The analysis of fruit quality suggested that compared with a storage temperature at 20 °C, a storage temperature of 0 °C results in CI in ‘Huangguan’ pear fruit, while a storage temperature of 10 °C and low temperature conditioning (LTC) alleviates the CI. Moreover, gene expression results indicated that the six PbDHNs were markedly enhanced at low temperatures, especially at 0 °C. The transcripts of PbDHN1, PbDHN4, PbDHN5 and PbDHN6 were also increased in the fruit stored at 10 °C, but they were lower than that at 0 °C except PbDHN5. Compared with low temperature storage at 0 °C, LTC treatment significantly depressed the expression of PbDHN1, PbDHN2, PbDHN3, PbDHN4, and PbDHN6, while enhanced the mRNA amount of PbDHN5. In conclusion, PbDHN1, PbDHN4, PbDHN5, and PbDHN6 were closely related to the CI, and LTC lowered the CI by down-regulating the expression of PbDHN1, PbDHN4, and PbDHN6 and by up-regulating PbDHN5 in ‘Huangguan’ pear fruit.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent chronic liver disorder with limited effective pharmacological treatments. Ziziphus jujuba Mill. leaves (ZJL) contain multiple bioactive compounds, but their effects on MASLD and underlying mechanisms remain unclear. Methods: The chemical constituents of ethanolic ZJL extract were characterized using UHPLC-Q-Orbitrap MS. A high-fat diet (HFD)-induced MASLD mouse model was used to evaluate its protective effects. Serum biochemical parameters, liver histopathology, and inflammatory indicators were assessed. Gut microbiota and hepatic metabolic alterations were investigated using 16S rDNA sequencing and untargeted metabolomics, respectively. Potential microbiota–metabolite associations and key regulatory targets were further explored by correlation analysis, molecular docking, and qRT-PCR. Results: Fifty-five compounds were identified in ZJL, mainly flavonoids, organic acids, and triterpenoids. ZJL treatment significantly reduced HFD-induced body weight gain, dyslipidemia, hyperglycemia, hepatic injury, inflammation, and lipid accumulation. ZJL also partially restored gut microbial homeostasis, particularly by decreasing the abundances of Blautia and Dorea. Metabolomic analysis indicated that glycerophospholipid metabolism was the major affected pathway, together with fatty acid biosynthesis and cytochrome P450-related metabolism. Microbial alterations were closely associated with lipid-related metabolites. Moreover, ZJL downregulated key genes, including Pla2g2a, Fasn, and Cyp2e1. Conclusions: ZJL alleviated HFD-induced MASLD, accompanied by coordinated alterations in gut microbiota composition, hepatic metabolism, and lipid-related gene expression, suggesting that these changes may contribute to its protective effects.