2. Academic Validation
  3. Propyl gallate mitigates diabetic liver injury via suppressing SLC7A11/GPX4-mediated hepatic ferroptosis and modulating gut-liver axis

Propyl gallate mitigates diabetic liver injury via suppressing SLC7A11/GPX4-mediated hepatic ferroptosis and modulating gut-liver axis

  • Biochem Pharmacol. 2026 Mar 22:249:117926. doi: 10.1016/j.bcp.2026.117926.
Zhaopeng Zhang 1,  Sue Jiao 2,  Han Wang 3,  Yang Chen 2,  Zhirun Zhang 2,  Ying Zhang 2,  Rui Gao 2,  Yunlong Xiao 2,  Yang Liu 4,  Yilong Zhu 5,  Guangze Zhu 6,  Junpeng Guo 7
Affiliations

Affiliations

  • 1 College of Pharmaceutical Sciences, Changchun University of Traditional Chinese Medicine, Changchun 130117, China.
  • 2 College of Integrated Traditional Chinese and Western Medicine, Changchun University of Traditional Chinese Medicine, Changchun 130117, China.
  • 3 Department of Clinical Laboratory, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun 130021, China.
  • 4 College of Clinical Medicine, Changchun Medical College, Changchun 130031, China.
  • 5 College of Integrative Medicine, Changchun University of Traditional Chinese Medicine, Changchun 130117, Jilin, China.
  • 6 Department of Clinical Laboratory, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun 130021, China. Electronic address: zhuguangze820@126.com.
  • 7 College of Clinical Medicine, Changchun University of Traditional Chinese Medicine, Changchun 130117, China. Electronic address: guojp1228@163.com.
PMID: 41876017 DOI: 10.1016/j.bcp.2026.117926
Abstract

Hepatic glycolipid metabolic dysregulation is a hallmark of type 2 diabetes mellitus (T2DM), with emerging evidence implicating Ferroptosis as a critical pathogenic mechanism. Propyl gallate (PG), a naturally occurring antioxidant, may counteract redox imbalance; however, its impact on Ferroptosis and gut-liver axis remains poorly understood. In this study, we investigated the protective effects of PG against high-fat diet (HFD)-induced diabetic liver injury in both in vivo and in vitro models. A combination of hepatic metabolomics, ferroptosis-related assays, and 16S rRNA Sequencing was employed. PG significantly reduced hepatic lipid accumulation and oxidative stress by inhibiting Ferroptosis, primarily through activation of the SLC7A11/GPX4 axis. Metabolomic analysis further demonstrated PG-mediated normalization of lipid peroxidation and glutathione metabolism in the liver. Notably, PG also enhanced intestinal barrier integrity by upregulating tight junction proteins (e.g., occludin, and ZO-1) and reshaping gut microbial composition, marked by increased abundance of beneficial genera such as Lactobacillus and Ruminococcus, known for their anti-inflammatory and antioxidant roles. Collectively, these findings suggest that PG ameliorates diabetic liver injury via dual mechanisms: (1) direct inhibition of SLC7A11/GPX4-dependent Ferroptosis and (2) indirect modulation of gut microbiota to preserve intestinal barrier function. This study positions PG as a promising candidate for T2DM therapy by targeting both hepatic redox imbalance and gut dysbiosis.

Keywords

Diabetes liver injury; Gut microbiota; Metabolomics; Propyl gallate; SLC7A11/GPX4.

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