Caprylic Acid Improves Lipid Metabolism, Suppresses the Inflammatory Response and Activates the ABCA1/p-JAK2/p-STAT3 Signaling Pathway in C57BL/6J Mice and RAW264.7 Cells.

Xin Sheng Zhang; Peng Zhang; Ying Hua Liu; Qing XU; Yong Zhang; Hui Zi LI; Lu Liu; Yu Meng Liu; Xue Yan Yang; Chang Yong Xue

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Caprylic Acid Improves Lipid Metabolism, Suppresses the Inflammatory Response and Activates the ABCA1/p-JAK2/p-STAT3 Signaling Pathway in C57BL/6J Mice and RAW264.7 Cells.

Author: Xin Sheng ZHANG ¹ ; Peng ZHANG ^{2
,

3} ; Ying Hua LIU ¹ ; Qing XU ¹ ; Yong ZHANG ¹ ; Hui Zi LI ⁴ ; Lu LIU ¹ ; Yu Meng LIU ¹ ; Xue Yan YANG ¹ ; Chang Yong XUE ¹
Author Information

1. Department of Nutrition, the First Medical Center of PLA General Hospital, Beijing 100853, China.
2. Department of Nutrition, the First Medical Center of PLA General Hospital, Beijing 100853, China
3. Guizhou Crops of Chinese Armed Police Force, Guiyang 550001, Guizhou, China.
4. Department of Nutrition, PLA Rocket Force Characteristic Medical Center, Beijing 100088, China.
Publication Type:Journal Article
Keywords: ATP binding cassette transporter A1; Caprylic acid; Inflammatory cytokine; Janus kinase 2; Signal transducer and activator of transcription 3
MeSH: ATP Binding Cassette Transporter 1/immunology*; Animals; Caprylates/chemistry*; Cholesterol/metabolism*; Diet, High-Fat/adverse effects*; Humans; Inflammation/metabolism*; Janus Kinase 2/immunology*; Lipid Metabolism/drug effects*; Macrophages/immunology*; Male; Mice; Mice, Inbred C57BL; RAW 264.7 Cells; STAT3 Transcription Factor/immunology*; Signal Transduction
From: Biomedical and Environmental Sciences 2022;35(2):95-106
CountryChina
Language:English
Abstract: OBJECTIVE:This study aimed to investigate the effects of caprylic acid (C8:0) on lipid metabolism and inflammation, and examine the mechanisms underlying these effects in mice and cells.
METHODS:Fifty-six 6-week-old male C57BL/6J mice were randomly allocated to four groups fed a high-fat diet (HFD) without or with 2% C8:0, palmitic acid (C16:0) or eicosapentaenoic acid (EPA). RAW246.7 cells were randomly divided into five groups: normal, lipopolysaccharide (LPS), LPS+C8:0, LPS+EPA and LPS+cAMP. The serum lipid profiles, inflammatory biomolecules, and ABCA1 and JAK2/STAT3 mRNA and protein expression were measured.
RESULTS:C8:0 decreased TC and LDL-C, and increased the HDL-C/LDL-C ratio after injection of LPS. Without LPS, it decreased TC in mice ( P < 0.05). Moreover, C8:0 decreased the inflammatory response after LPS treatment in both mice and cells ( P < 0.05). Mechanistic investigations in C57BL/6J mouse aortas after injection of LPS indicated that C8:0 resulted in higher ABCA1 and JAK2/STAT3 expression than that with HFD, C16:0 and EPA, and resulted in lower TNF-α, NF-κB mRNA expression than that with HFD ( P < 0.05). In RAW 264.7 cells, C8:0 resulted in lower expression of pNF-κBP65 than that in the LPS group, and higher protein expression of ABCA1, p-JAK2 and p-STAT3 than that in the LPS and LPS+cAMP groups ( P < 0.05).
CONCLUSION:Our studies demonstrated that C8:0 may play an important role in lipid metabolism and the inflammatory response, and the mechanism may be associated with ABCA1 and the p-JAK2/p-STAT3 signaling pathway.