Protective Role of Mytilus edulis Hydrolysate in Lipopolysaccharide-Galactosamine Acute Liver Injury

Acute liver injury in its terminal phase trigger systemic inflammatory response syndrome with multiple organ failure. An uncontrolled reaction is difficult to treat and contributes high mortality. Therefore, solve this problem a search for new therapeutic approaches remains urgent. This study aimed explore the protective effects of M. edulis hydrolysate (N2-01) against Lipopolysaccharide-D-Galactosamine (LPS/D-GalN)-induced murine acute injure underlying mechanisms. N2-01 analysis, using Liquid Chromatography Mass Spectrometry (LCMS) metabolomic proteomic platforms, confirmed composition, molecular-weight distribution, reproducibility between manufactured batches. efficiently protected mice LPS/D-GalN-induced injury. The most prominent result (100% survival rate) was obtained by constant subcutaneous administration small doses drug. decreased Vascular Cell Adhesion Molecule-1 (VCAM-1) expression from 4.648 ± 0.445 1.503 0.091 Mean Fluorescence Intensity (MFI) Interleukin-6 (IL-6) production activated Human Umbilical Vein Endothelial Cells (HUVECs) 7.473 0.666 2.980 0.130 ng/ml vitro . drug increased Nitric Oxide (NO) HUVECs 27.203 2.890 69.200 4.716 MFI but significantly inducible Synthase (iNOS) 24.030 2.776 15.300 1.290 NO peritoneal lavage cells 6.777 0.373 µm 2.175 0.279 µm. capability preparation enhance endothelium barrier function reduce vascular permeability Electrical Cell-substrate Impedance Sensor (ECIS) test Miles assay vivo These results suggest as promising agent treating wide range conditions associated inflammation endothelial dysfunction.