NEW ARTICLE FROM IBG ON THE MECHANISM OF NEUROPROTECTION
Researchers of the Neurodegeneration and Neuroprotection Lab at IBG published their latest study on the mechanism of ethyl pyruvate’s anti-inflammatory neuroprotective effect in the journal Antioxidants.
Ethyl pyruvate (EP) is a stable form of the pyruvate molecule that protects tissues from the adverse effects of inflammation. It has been shown to improve the prognosis of neurodegenerative disorders, such as Alzheimer’s and Parkinson’s Diseases, in rodents models.
Prof. Dr. Şermin Genç, group leader of the Neurodegeneration and Neuroprotection Lab at IBG, her group members Dr. Melis Olçum, Devrim Yağmur Durur and Bora Taştan, as well as their collaborators from Dokuz Eylül University (İrem Nur Gökbayrak and Prof. Dr. Kürşad Genç) and Izmir Democracy University (Dr. Kemal Uğur Tüfekci) investigated the anti-inflammatory effects of EP in human microglial cells.
Microglial cells are the primary immune components of the central nervous system (CNS). They initiate the inflammatory response upon exposure to a threat, such as prion proteins, by activating their inflammasomes. Inflammasomes are the complex molecules that induce cytokines and cell death in response to inflammation. Prof. Dr. Genç and her collaborators observed that EP suppressed NLRP3 inflammasome activation, decreased the secretion of cytokines and reduced the level of pyroptotic cell death resulting from inflammasome activation. Furthermore, EP also decreased the level of reactive oxygen species (ROS) in microglial cells. Their results showed, for the first time, the fact that EP suppressed inflammation via miR-223 regulation on the NF-κB/HMGB1 axis.