ABSTRACT
Emerging evidence suggests that sea cucumber ether phospholipids (ether-PLs) can modulate high-fat diet (HFD)-induced metabolic disorders. However, whether this modulation is associated with metabolic pathways related to oxidative stress and inflammation remains unclear. This study aimed to investigate the antioxidative and anti-inflammatory effects on HFD-fed mice and the associated metabolism pathways in response to administration with sea cucumber ether-PLs using integrated biochemistry and a metabolomics approach. Biochemistry analysis and histological examinations showed that sea cucumber ether-PLs significantly decreased body weight gain and fat deposition in tissues. PE-P was superior to PC-O in alleviating reactive oxygen species (ROS), malondialdehyde (MDA) and inflammatory responses (IL-6, TNF-α and MCP-1) in the HFD-induced mouse model. Serum metabolomics analysis revealed that it upregulated four metabolites and downregulated twenty-four metabolites compared to those in HFD mice after ether-PL administration. Pathway analysis indicated that sea cucumber ether-PLs alleviate the HFD-induced inflammation and oxidative stress by three main metabolic pathways, namely fatty acid metabolism, branched-chain amino acid (BCAA) metabolism, and trichloroacetic acid (TCA) metabolism. Taken together, sea cucumber ether-PLs showed great potential to become a natural functional food against oxidative stress and inflammation caused by HFD.
Subject(s)
Diet, High-Fat , Sea Cucumbers , Amino Acids, Branched-Chain/metabolism , Animals , Anti-Inflammatory Agents/pharmacology , Diet, High-Fat/adverse effects , Fatty Acids/pharmacology , Inflammation/drug therapy , Inflammation/metabolism , Interleukin-6/metabolism , Malondialdehyde , Mice , Mice, Inbred C57BL , Oxidative Stress , Phospholipid Ethers/pharmacology , Phospholipid Ethers/therapeutic use , Reactive Oxygen Species , Sea Cucumbers/metabolism , Trichloroacetic Acid/pharmacology , Trichloroacetic Acid/therapeutic use , Tumor Necrosis Factor-alpha/metabolismABSTRACT
Antarctic krill oil (AKO) is usually encapsulated by the protein materials, enhancing its oxidative stability. Proteins exhibit immense effect on lipid oxidation and induce protein-lipid co-oxidation. This study aimed at elucidating the co-oxidation mechanism of AKO and whey protein (WP) or myofibrillar protein (MP) in oil-in-water emulsions. The estimations of malondialdehyde (MDA) content, phospholipid molecular species, and pyrrole content resulted in increased and decreased oxidation rate of AKO (especially phosphatidylethanolamine) by WP and MP, respectively. Meanwhile, protein concentration, sulfhydryl content, the loss of tryptophan fluorescence intensity, and sodium dodecyl sulfate-polyacrylamide gel electrophoresis results demonstrated that AKO promoted WP oxidation but inhibited MP oxidation. Further, the antioxidative abilities of seven common antioxidants were evaluated. Ascorbyl palmitate showed the most substantial antioxidative effect for both AKO and proteins (about 70% decrease of MDA content and 30% decrease of the decrease ratio of tryptophan fluorescence intensity). This finding supported that different proteins could exhibit different pro/anti-oxidative effects on lipid oxidation, especially for marine lipids abundant in phospholipids and polyunsaturated fatty acids. Besides, MP could also act as antioxidant in MP AKO emulsions, further extending its application from traditional surfactants. PRACTICAL APPLICATION: AKO is usually encapsulated by the protein materials, enhancing its oxidative stability. The results demonstrated MP could inhibit AKO oxidation, and vice versa, especially when ascorbyl palmitate was added at the same time. As a result, this finding explored a new potential wall material with antioxidative ability for the encapsulated products of AKO.
