[Analysis of serum lipidomics for a spontaneous hepatic fibrosis mouse model].

Objective: To construct Slc27a5 gene knockout mice and investigate changed conditions in the serum lipidomics. Methods: Liver tissues and serum samples were collected from wild-type and Slc27a5 gene knockout mice at different time points. Hematoxylin-eosin staining was used to observe hepatic pathological changes. Immunofluorescence staining was used to detect the expression of α-smooth muscle actin and F4/80 proteins. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to analyze changes in serum lipid composition. The comparison of quantitative data was performed using the t-test between groups. Results: The percentage area of α-smooth muscle actin staining (7.33% ± 3.08% vs. 1.14% ± 0.30%, t=3.996, P<0.01) and F4/80 staining area (2.48% ± 0.71% vs. 0.76% ± 0.19%, t=4.683, P<0.01) was significantly higher in Slc27a5 gene-deficient mice than in wild-type mice in liver tissue at 24 months of age. The results of the serum lipidomics analysis indicated significant alterations in lipid composition of Slc27a5 gene-deficient mice. Compared with wild-type mice, the serum of Slc27a5 gene-deficient mice had increased levels of 19 types of phosphatidylinositols and 14 types of phosphatidylcholines and decreased levels of 17 types of phosphatidylethanolamines. Conclusion: Spontaneous liver fibrosis induced by Slc27a5 deficiency in a mouse model is accompanied by significant remodeling of the serum lipid profiles.