Dietary Ethanolamine Glycerophospholipids Alleviate Acute Hepatic Injury in Mice: A Comparison of Two Subclasses

Ethanolamine plasmalogen (PlsEtn) is a subclass of ethanolamine glycerophospholipids (EtnGpls) that has been reported to exhibit physiological and nutritional hepatic functions. However, the effects of dietary PlsEtn on acute liver injury remain unclear. In the present study, we investigated the dietary effects of PlsEtn on acute hepatic injury in mice treated with an intraperitoneal injection of lipopolysaccharide and d-galactosamine (LG). The results obtained after administering the PlsEtn-rich diet were compared with those obtained after administration of a phosphatidylethanolamine (PtdEtn)-rich diet, a major subclass of hepatic EtnGpls. Dietary EtnGpl rich in PlsEtn or PtdEtn suppressed the LG-induced increase in plasma aspartate aminotransferase activity, which is a marker of liver cell injury. In the livers of LG-treated mice, the PlsEtn-rich diet suppressed the expression of cleaved caspase-3, an effector caspase for apoptosis, whereas the PtdEtn-rich diet suppressed p53 expression and maintained B-cell lymphoma 2 expression. Additionally, the PlsEtn-rich diet increased the ratio of docosahexaenoic acid, an anti-inflammatory factor, to total fatty acids in the livers of LG-treated mice, whereas this effect was not observed in mice fed the PtdEtn-rich diet. These results suggest that dietary EtnGpls alleviate acute hepatic injury; however, the mechanism of suppression may differ depending on its subclass.

Practical applications: Analyzing the beneficial effects of PlsEtn and PtdEtn, both subclasses of EtnGpl, contributes to understanding the protective mechanisms of glycerophospholipids against hepatic injuries. Although the concentration of PlsEtn in the liver is less than one-tenth that of PtdEtn, endogenous PlsEtn has been reported to exhibit anti-inflammatory effects and improve lipid metabolism in the liver. Consequently, both dietary PlsEtn and PtdEtn demonstrate significant hepatic protection; however, their mechanisms of suppression differ. These findings suggest that the structural characteristics of PlsEtn and PtdEtn, which are responsible for hepatic protection, vary.