Suppressive effects of an apoptotic mimicry prepared from jumbo-flying squid-skin phospholipids on the osteoclastogenesis in receptor activator of nuclear factor kappa B ligand/macrophage colony-stimulating factor-induced RAW 264.7 cells
Journal
Journal of the Chinese Medical Association
Journal Volume
84
Journal Issue
1
Pages
51-60
Date Issued
2021
Author(s)
Abstract
Background: Liposomes containing docosahexaenoic acid (DHA) and phosphatidylserine were claimed to inhibit osteoclast formation and bone resorption in the inflammatory status. Herein, we proposed that an apoptotic mimicry (SQ liposome) prepared from squid-skin phospholipids can explore the suppressive osteoclastogenesis. Methods: The intermolecular fatty-acid composition in the phospholipid of squid-skin extract was analyzed by GC-FID. The SQ liposome structure was characterized by size distribution and zeta potential (ζ). RAW 264.7 cell is used to study the effect of SQ liposomes on osteoclast differentiation. Secretion of prostaglandin E2 (PGE2) and transforming growth factor-β (TGF-β) from RAW 264.7 cells were assayed. Antiosteoclastogenesis effects were performed via the tartrate-resistant acid phosphatase (TRAP)positive multinucleated cell (MNC) counting, bone resorption pit assay, and TRAP activity analysis. The specific gene expressions related to antiosteoclastogenesis were also detected. Results: An apoptotic mimicry through the use of a single-layer liposome (SQ liposome) with phosphatidylserine exposure contains DHA (28.7%) and eicosapentaenoic acid (EPA, 11.8%). Co-treatment with receptor activator of nuclear factor kappa B ligand (RANKL)/macrophage colony-stimulating factor induced RAW 264.7-cell differentiation into mature osteoclasts, thus enhancing PGE2 and TGF-β secretion. However, cotreatment with 1 mg/mL of SQ liposome restored (p < 0.05) the cell viabilities under the RANKL stress. Increased PGE2 levels was downregulated (p < 0.05) in cotreatments with 0.11 and 0.33 mg/mL of SQ liposome, but on the TGF-β levels were not (p > 0.05) influenced in SQ liposome cotreatments. Cotreatments with 0.33–1 mg/mL of SQ liposome suppressed (p < 0.05) the osteoclast maturation (such as decreased MNCs and bone pit formation), inhibited TRAP activities, and downregulated the osteoclastogenesis-related gene expressions. Conclusion: In summary, current data support that a possible prevention of our prepared SQ liposomes which are rich in DHA and EPA on bone loss is through the suppression of osteoclastogenesis. Moreover, based on the results from this study an in vivo study warrants a further investigation. Copyright ? 2020, the Chinese Medical Association.
Subjects
acid phosphatase tartrate resistant isoenzyme; cathepsin K; colony stimulating factor 1; docosahexaenoic acid; gelatinase B; icosapentaenoic acid; liposome; osteoclast differentiation factor; palmitic acid; phosphatidylserine; prostaglandin E2; sq liposome; transforming growth factor beta; unclassified drug; animal cell; animal tissue; apoptosis; Article; cell counting; cell differentiation; cell viability; controlled study; cytotoxicity; Dosidicus gigas; down regulation; enzyme activity; flame ionization detection; gas chromatography; gene expression; lipid composition; multinuclear cell; nonhuman; osteoclast; osteoclastogenesis; osteolysis; particle size; protein secretion; RAW 264.7 cell line; skin; zeta potential
SDGs
Type
journal article