Experimental findings show TRLW-2 agonist enhances pregnane X receptor activity in murine models of ulcerative colitis, suggesting a novel therapeutic approach.
Background The therapeutic development of pregnane X receptor (PXR) agonists for ulcerative colitis (UC) is hindered by the poor selectivity of the canonical ligand-binding pocket. This study aimed to identify a novel, selectivity-enhancing binding site on PXR and a corresponding natural ligand for UC treatment. Methods A distinct binding pocket (Pocket 1–5) within the PXR ligand-binding domain was identified using a multi-algorithm computational approach (SiteMap, Fpocket, Prank, CASTpFold). Structure-based virtual screening of 6,058 natural compounds from a traditional Chinese medicine library was performed via Glide docking (High-Throughput Virtual Screening/Standard Precision/Extra Precision modes, HTVS/SP/XP), with binding affinities refined by molecular mechanics/generalized Born surface area (MM/GBSA). The top candidate, TRLW-2 (catechin), was evaluated using luciferase reporter assays, quantitative real-time PCR (Qpcr), and functional assays (CCK-8, EdU, Annexin V-FITC/PI) in HEK293T and mouse colonic epithelial cells (MCECs). In vivo efficacy was assessed in a DSS-induced murine colitis model. Results TRLW-2 exhibited high affinity for pocket 1-5, forming key hydrogen bonds with residues including Ser350, Asp352, Asp363, Thr398, and Arg401, which was validated by molecular dynamics simulations (MD) and site-directed mutagenesis. Functionally, TRLW-2 acted as a potent PXR agonist, significantly upregulating detoxifying enzymes (such as Cyp2b10, Cyp3a11 and Ugt1a1) and proliferation markers (PCNA, CDK1, Cyclin B1, and Ki67) in vitro . It promoted epithelial cell proliferation and inhibited apoptosis in MCECs. In DSS-induced colitis mice, TRLW-2 treatment significantly attenuated weight loss, reduced disease activity index DAI) and colonic mucosa damage index (CMDI) scores, ameliorated colon shortening, and improved histopathology. Conclusion This study identified pocket 1–5 as a selectivity-enhancing site on PXR. The natural product TRLW-2, discovered via virtual screening, potently engages this pocket and demonstrates robust anti-inflammatory and mucosal healing effects, validating a promising strategy for developing precision therapeutics for UC.
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Rao et al. (2025) studied this question.
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