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Ethanol extract of Polygonum perfoliatum L. alleviates inflammation and ferroptosis in ulcerative colitis
Wenze Wu1, Shaowen Tan1, Qingqi Meng1
1Key Laboratory of Bioresource Research and Development of Liaoning Province, College of Life and Health Sciences, National Frontiers Science Center for Industrial Intelligence and Systems Optimization, Key Laboratory of Data Analytics and Optimization for Smart Industry, Ministry of Education, Northeastern University, Shenyang 110169, China.
Background:
Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by relapsing episodes and mucosal damage. Polygonum perfoliatum L. (gangbangui, GBG), known for its heat-clearing and detoxifying effects, has traditionally been used to treat inflammatory conditions, but its efficacy in UC remains unclear.
Purpose:
This study aimed to investigate the pharmacological mechanisms of the ethanol extract of GBG (EEGBG) in UC.
Methods:
The protective effects of EEGBG were evaluated in a dextran sulfate sodium (DSS)-induced colitis model in C57BL/6 mice and LPS-stimulated RAW 264.7 macrophages. Metabolomics, network pharmacology, and multiple assays-including Western blot, RT-qPCR, histopathology, immunofluorescence, and gene knockdown-were employed to elucidate the underlying mechanisms.
Results:
EEGBG treatment significantly prevented DSS-induced body weight loss, decreased disease activity index (DAI) scores, restored mucosal architecture, and reduced inflammatory cell infiltration. Metabolomics revealed that EEGBG treatment modulated metabolites involved in anti-inflammatory and antioxidant processes, immune regulation, barrier integrity, energy metabolism, and tissue repair. Network pharmacology suggested that EEGBG protects against UC through anti-inflammatory and antioxidant activities, including ferroptosis inhibition. Mechanistic studies confirmed that EEGBG regulated the NF-κB and Nrf2 signaling pathways, thereby suppressing inflammation and ferroptosis-associated oxidative stress. Additionally, EEGBG preserved mitochondrial function by maintaining redox balance and structural stability. Notably, Nrf2 knockdown abolished these protective effects, highlighting the pivotal role of Nrf2 in mediating EEGBG's bioactivity.
Conclusions:
This study reveals that EEGBG protects against UC by modulating both inflammatory and oxidative stress pathways. EEGBG treatment decreased NF-κB pathway activity and increased Nrf2 pathway activation, which contributes to its anti-inflammatory and antioxidant effects. These findings identify EEGBG as a promising multi-target therapeutic candidate for UC and provide novel mechanistic insights into disease management.
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