1. Academic Validation
  2. Glycine tabacina extract alleviates inflammatory bowel disease via NF-κB, JNK and Nrf2 signaling pathways

Glycine tabacina extract alleviates inflammatory bowel disease via NF-κB, JNK and Nrf2 signaling pathways

  • J Ethnopharmacol. 2025 May 12:347:119744. doi: 10.1016/j.jep.2025.119744.
Yongkai Liang 1 Zhimin Miao 1 Junming Chen 1 Lihua Tan 1 Yuxin Zhao 1 Xiaobing Cui 1 Jinmiao Zhong 1 Ruting Zhong 1 Wendi Yue 1 Boyang Qiu 1 Hua Yu 2 Chengwei He 3
Affiliations

Affiliations

  • 1 State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Taipa, Macao SAR, 999078, China.
  • 2 State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Taipa, Macao SAR, 999078, China; Department of Pharmaceutical Science, Faculty of Health Sciences, University of Macau, Taipa, Macao SAR, 999078, China.
  • 3 State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Taipa, Macao SAR, 999078, China; Department of Pharmaceutical Science, Faculty of Health Sciences, University of Macau, Taipa, Macao SAR, 999078, China. Electronic address: chengweihe@um.edu.mo.
Abstract

Ethnopharmacological relevance: Inflammatory bowel diseases (IBD) are chronic inflammatory disorders of the colon, often triggered by unhealthy diets, infections, and dysregulated immune responses. Current treatments for IBD are limited by relapse, drug resistance, side effects, and high costs. Glycine tabacina (Labill.) Benth, a legume native to southeastern China, has traditionally been used for its medicinal properties in treating rheumatoid arthritis, nephritis, and osteoporosis. However, its effects on IBD remain unexplored.

Aim of the study: This study aimed to investigate the anti-colitis effects and underlying mechanisms of Glycine tabacina ethanol extract (GTE) using in vitro and in vivo models.

Materials and methods: The chemical components of GTE were identified using high-performance liquid chromatography (HPLC). The effects of GTE on lipopolysaccharide (LPS)-induced inflammation and oxidative stress were assessed in Caco-2 cells. Dextran sulfate sodium (DSS)-induced colitis in mice was used to evaluate GTE's therapeutic potential. ELISA, RT-qPCR, immunofluorescence, and immunoblotting were performed to measure gene expression and signaling pathway activity. Histological analysis of colon tissues was conducted using H&E staining.

Results: GTE significantly reduced LPS-induced inflammation and oxidative stress in Caco-2 cells and alleviated DSS-induced colitis in mice. Mechanistically, GTE decreased pro-inflammatory cytokines, Matrix Metalloproteinases (MMPs), and Reactive Oxygen Species (ROS), while improving intestinal barrier integrity. Furthermore, GTE suppressed the NF-κB and MAPK/JNK pathways while activating the Nrf2 pathway. These results suggest that GTE may serve as a promising therapeutic agent for IBD by modulating key inflammatory and oxidative stress pathways.

Conclusions: The anti-inflammatory and antioxidant properties of GTE mitigated intestinal epithelial cell damage by preserving tight junction proteins and maintaining intestinal barrier integrity. Given its high efficacy and favorable safety profile, GTE represents a promising therapeutic candidate for managing chronic and refractory inflammatory disorders such as IBD.

Keywords

Glycine tabacina; Inflammatory bowel disease; Intestinal barrier integrity; MAPK/JNK pathway; NF-κB pathway; Nrf2 pathway.

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