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Plasmalogens Reversed Oxidative Stress and Inflammatory Response Exacerbated by Damage to Cell Membrane Properties in Acute Liver Injury.
J Agric Food Chem
December 2024
School of Food Science and Technology, Jiangnan University, Wuxi, Jiangsu Province 214122, People's Republic of China.
Background: In acute liver injury (ALI), cell membrane damage could induce an inflammatory response and oxidative stress. As a membrane glycerophospholipid, plasmalogens (PLS) are crucial in regulating the cell membrane properties and exhibit beneficial effects in various liver diseases. However, the specific regulatory effects of PLS in the ALI remain unknown.
View Article and Find Full Text PDFsurface components and DKK1 signalling via LRP6 promote migration and longevity of neutrophils in the infection site.
Front Immunol
November 2024
Department of Pathology, Microbiology, and Immunology, University of Nebraska Medical Center, Omaha, NE, United States.
Background: Host-related factors highly regulate the increased circulation of neutrophils during infection. Platelet-derived Dickkopf-1 (DKK1) is established as a high-affinity ligand to LRP6. Recently, we demonstrated that DKK1 upregulates leukocyte-platelet aggregation, infiltration of neutrophils to the draining lymph node and Th2 differentiation during infection, suggesting the potential involvement of the DKK1-LRP6 signalling pathway in neutrophil migration in infectious diseases.
View Article and Find Full Text PDFThe beneficial effects of a formulated supplement of plasmalogen and elastin on the memory function in healthy elderly subjects were investigated by a randomized, double-blind, placebo-controlled, parallel-group analysis. Plasmalogen has been shown to exert beneficial effects on cognitive function in animal models and human clinical trials, while elastin improves vascular elasticity and increases blood flow. The levels of plasmalogen and elastin decreases with aging.
View Article and Find Full Text PDFMaternal obesity puts the offspring at high risk of developing obesity and cardio-metabolic diseases in adulthood. Here, using a mouse model of maternal high-fat diet (HFD)-induced obesity, we show that whole body fat content of the offspring of HFD-fed mothers (Off-HFD) increases significantly from very early age when compared to the offspring regular diet-fed mothers (Off-RD). We have previously shown significant metabolic and immune perturbations in the bone marrow of newly-weaned offspring of obese mothers.
View Article and Find Full Text PDFTafazzin deficiency causes substantial remodeling in the lipidome of a mouse model of Barth Syndrome cardiomyopathy.
Front Mol Med
April 2024
Institute of Anatomy and Cell Biology, University of Würzburg, Würzburg, Germany.
Barth Syndrome (BTHS) is a rare X-linked disease, characterized clinically by cardiomyopathy, skeletal myopathy, neutropenia, and growth retardation. BTHS is caused by mutations in the phospholipid acyltransferase tafazzin (Gene: TAFAZZIN, TAZ). Tafazzin catalyzes the final step in the remodeling of cardiolipin (CL), a glycerophospholipid located in the inner mitochondrial membrane.
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