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Ethyl pyruvate (EP) has potent influence on redox processes, cellular metabolism, and inflammation. It has been intensively studied in numerous animal models of systemic and organ-specific disorders whose pathogenesis involves a strong immune component. Here, basic chemical and biological properties of EP are discussed, with an emphasis on its redox and metabolic activity. Further, its influence on myeloid and T cells is considered, as well as on intracellular signaling beyond its effect on immune cells. Also, the effects of EP on animal models of chronic inflammatory and autoimmune disorders are presented. Finally, a possibility to apply EP as a treatment for such diseases in humans is discussed. Scientific papers cited in this review were identified using the PubMed search engine that relies on the MEDLINE database. The reference list covers the most important findings in the field in the past twenty years.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8742706 | PMC |
http://dx.doi.org/10.1007/s00011-021-01529-z | DOI Listing |
Front Pharmacol
August 2025
Senior Department of Burns & Plastic Surgery, Institute of Burn in the Fourth Medical Centre, Chinese PLA General Hospital, Beijing, China.
Background/objectives: Burns can cause severe physiological disturbances. Oral rehydration therapy (ORT) is an alternative to intravenous fluids. However, the World Health Organization-recommended oral rehydration solution (WHO-ORS) lacks specific components to address the critical physiological changes in patients with burns.
View Article and Find Full Text PDFBiochim Biophys Acta Mol Cell Res
July 2025
Department of Gastroenterology, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address:
In the intricate process leading to liver fibrosis, which frequently correlates with inflammation, the activation of hepatic stellate cells (HSCs) is critical. High mobility group box 1(HMGB1), as endogenous danger signal in the extracellular environment, governs the activation of caspase-1 and hepatic stellate cell. Constructing a liver fibrosis model via intraperitoneal thioacetamide (TAA) administration unveiled excessive HMGB1 expression and serum release during the TAA-induced fibrosis progression.
View Article and Find Full Text PDFToxics
May 2025
School of Public Health, Hangzhou Medical College, Hangzhou 310013, China.
Malignant mesothelioma (MM) is a highly aggressive cancer strongly associated with asbestos exposure, and accumulating evidence suggests that high mobility group box 1 (HMGB1) plays a central role in its pathogenesis. Our in vitro and in vivo experiments revealed that HMGB1 was highly expressed in MM. Both genetic and pharmacological inhibition of HMGB1 markedly suppressed MM cell viability, migration, and invasion, while inducing G1-phase cell cycle arrest and enhancing apoptosis.
View Article and Find Full Text PDFReprod Sci
June 2025
Department of Medical Biotechnology, Gujrat Biotechnology University, Gandhinagar, 382355, Gujrat, India.
Endometriosis is a disease where vascularised tissue similar to endometrium (the lining of the uterus) grows outside of the uterus. Its pathogenesis involves a complex interplay of inflammation, angiogenesis, cellular proliferation, reactive oxygen species (ROS) production, altered energy metabolism, and epithelial-to-mesenchymal transition (EMT).Even though endometriosis was described more than 150 years ago, we have been unable to find its effective therapy.
View Article and Find Full Text PDFEur J Pharmacol
July 2025
Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University, 3-4-1 Kowakae, Higashi-Osaka, 577-8502, Japan. Electronic address:
High mobility group box1 (HMGB1), a nuclear protein, once acetylated by histone acetyltransferase, is released into the extracellular space, and causes pain signals, thereby contributing to pathological pain. Repeated intracolonic administration of butyrate, known to inhibit histone deacetylase (HDAC), produces colonic hypersensitivity in rodents, being widely used as models for irritable bowel syndrome (IBS). Thus, we asked whether HMGB1 would participate in the butyrate-induced colonic hypersensitivity in mice, and analyzed the underlying mechanisms.
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