To die or not to die? Modulating ferroptosis in liver fibrosis using PPC-rich lipid as bioactive excipients in tablets

Yasmin Jokar, MSc. – Master Student, Department of Chemistry, Biochemistry and Pharmaceutical Sciences, University of Bern; Simone Aleandri – Senior Scientist, Department of Chemistry, Biochemistry and Pharmaceutical Sciences, University of Bern; Solveigh Cornelia Koeberle, Dr.rer.nat. – Principal Investigator, Institute of Pharmaceutical Sciences / Pharmacognosy, University of Graz; Andreas Koeberle, Prof.Dr. – Full Professor and the head of the Pharmacognosy, Institute of Pharmaceutical Sciences / Pharmacognosy, University of Graz; Paola Luciani, Prof.Dr. – Full Professor of Pharmaceutical Technology, Department of Chemistry, Biochemistry and Pharmaceutical Sciences, University of Bern

Introduction:

Ferroptosis is an iron-dependent, non-apoptotic cell death program initiated by excessive lipid peroxidation¹. Hepatic stellate cells (HSCs), the primary drivers of fibrosis, stand out as key targets for cell-death-based therapies²'³. Previously, we showed that the polyenylphosphatidylcholine-rich soy phospholipid complexed with MgCl₂, Soluthin^® S80 M, has significant antifibrotic potential⁴. This study investigates whether the modulation of ferroptosis is a mechanism underlying the antifibrotic effects of S80 M in LX-2 cells.