Liquiritigenin

Drought stress poses a major challenge to global crop yields, necessitating the identification of drought-responsive genes essential for improving plant tolerance and productivity under water deficit conditions. UDP-glycosyltransferases are key enzymes that modulate plant metabolism through glycosylation, playing a critical role in coping with environmental stresses. In this study, we functionally characterized a flavonoid/triterpene glucosyltransferase gene, UGT73B34, from Glycyrrhiza glabra, induced by osmotic stress. Transgenic Nicotiana tabacum plants overexpressing GgUGT73B34 exhibited significantly enhanced growth and survival under drought mediated through an ABA-independent mechanism. The OE-6 line of GgUGT73B34 plants exhibited superior water retention, reduced stomatal apertures, low reactive oxygen species and decreased transpiration rates compared to wild-type controls. These physiological advantages correlated with elevated accumulation of flavonoids, phenolics, proline, soluble sugars, and indole-3-acetic acid. Gene expression analysis revealed downregulation of ABA-dependent drought-responsive genes (ABI4, ABI5, ERD10a) and antioxidant enzymes (APX, GST, CAT2, PRX), while strongly inducing ABA-independent regulators DREB3 and SnRK2.1, indicating a strategic shift toward sustained drought resilience. Homology-model based structure analysis revealed a conserved GT-B fold with flexible substrate-binding domains, enabling broad specificity for diverse metabolites interacting predominantly with His and Glu as key amino acid residues. In vitro enzymatic assays confirmed mono- and di-glycosylation of glabridin, liquiritigenin, licochalcone A, and 18α-glycyrrhetinic acid as validated by LC-MS/MS analysis. Our findings demonstrated that GgUGT73B34 confers drought tolerance through coordinated regulation of osmoregulation, antioxidant capacity, and hormone homeostasis via an ABA-independent pathway, providing valuable insights for developing drought-resilient crops and for engineering enhanced production of bioactive natural products.

It has been shown that a high-salt diet (HSD) significantly damages the colonic epithelial barrier, resulting in increased intestinal permeability, upset gut microbial balance, and generalized inflammation. Despite this, effective therapeutic strategies to prevent HSD-induced intestinal damage remain limited. This study aims to explore the preventive properties and basic mechanisms of liquiritigenin (LG)，a natural flavonoid, against chronic colonic injury induced by prolonged HSD exposure. A murine model of chronic colitis was established by administering an 8 % NaCl diet, and LG therapy was used to evaluate how it affected the function of the intestinal barrier and allergic reactions. The development of pro- and anti-inflammatory cytokines (il-β, il-6, tnf-α, il-10, and inos) as well as important tight junction proteins (ZO-1, Claudin-3, and Occludin) was assessed. Furthermore, we investigated the molecular processes in vitro using normal colonic epithelial cell line NCM-460, with particular focus on the NF-κB and JAK/STAT3 signaling pathways. LG increased the expression of junction-binding proteins, greatly enhanced the intestinal wall integrity, and mitigated histopathological damage. Furthermore, it markedly attenuated excessive inflammatory responses both in vivo and in vitro. Mechanistically, LG suppressed the phosphorylation of key components within the pathways of JAK/STAT3 and NF-κB, thereby inhibiting downstream inflammatory signaling and epithelial cell injury. Collectively, these results demonstrate that liquiritigenin exerts protective effects against HSD-induced colonic damage by concurrently modulating the NF-κB and JAK/STAT3 pathways, highlighting its therapeutic potential for high salt-related intestinal disorders.