Exogenous Quercetin Enhances Salt Tolerance in Apocynum venetum Seedlings: Insights From Physiology and Transcriptomic Regulation.

Soil salinization severely constrains crop yields and quality. Apocynum venetum L. is an important halophytic plant; however, its young seedlings exhibit limited salt tolerance. To elucidate the mechanism by which exogenous quercetin alleviates salt stress in A. venetum seedlings. The present work integrates phenotypic observation, physiological measurement, and transcriptome analysis. There were four treatment groups: HCK (control), HCKN (salt stress), Q3 (quercetin), and Q3 + N (quercetin + salt stress). These findings demonstrated that under salt stress, exogenous quercetin significantly improved phenotypic traits, including plant height, stem, root, and leaves. Quercetin application reduced malondialdehyde (MDA) content to maintain cell membrane stability and restore the photosynthetic system. It also enhanced the activities of superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT), thereby promoting the accumulation of proline and soluble proteins and alleviating salt stress damage. Transcriptomic analysis identified 21 differentially expressed genes (DEGs) modulated by quercetin to alleviate salt stress. These DEGs were enriched in pathways associated with glycerophospholipid metabolism, plant hormone signal transduction, and secondary metabolite biosynthesis. Notably, genes such as PIOX (flavonoid synthase) and TPPD (terpenoid phenol synthase) were specifically up-regulated. This upregulation facilitates the synthesis of salt-stress-mitigating secondary metabolites, including flavonoids and terpenoids, which contribute to reducing reactive oxygen species (ROS) and, subsequently, alleviate oxidative damage. The reliability of the RNA-seq data was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR). Collectively, these findings demonstrated that quercetin alleviates salt stress through a dual mechanism: enhancing antioxidant defenses and modulating key molecular pathways.