Poly-IC와 리포테이코산으로 유발되는 마우스 대식세포의 산화 스트레스 반응에 미치는 에모딘의 영향과 관련된 표적단백질 탐색

초록

This study aimed to investigate the antioxidative effects of emodin (EM) on macrophages stimulated with pathogen-associated molecular patterns, including polyinosinic–polycytidylic acid (poly-IC) and lipoteichoic acid. RAW 264.7 mouse macrophages co-stimulated with poly-IC and lipoteichoic acid were treated with EM (25 or 50 µM) for 16–26 h, and hydrogen peroxide production was quantified using the dihydrorhodamine-123 assay. Nitric oxide production was evaluated in poly-IC–stimulated THP-1 human monocytes treated with EM (5–50 µM) using the Griess reagent. Additionally, molecular docking analysis was conducted using AutoDock Vina to assess the binding affinity of EM toward 12 protein targets associated with oxidative stress and inflammatory signaling. EM significantly inhibited hydrogen peroxide production in poly-IC and lipoteichoic acid–stimulated RAW 264.7 macrophages across all incubation periods (16–26 h), demonstrating a sustained antioxidative effect. EM also dose-dependently reduced nitric oxide production in poly-IC–stimulated THP-1 monocytes. Consistently, molecular docking revealed strong binding affinity of EM toward multiple oxidative stress– and inflammation-related protein targets, supporting its potential multi-target mechanism. EM exerts antioxidative activity by suppressing hydrogen peroxide and nitric oxide production in stimulated macrophages, and its multi-target binding profile suggests a mechanistic basis for its redox-regulatory and anti-inflammatory potential.

키워드