Home > Journals > Minerva Medica > Past Issues > Minerva Medica 2019 April;110(2) > Minerva Medica 2019 April;110(2):107-14

CURRENT ISSUE
 

JOURNAL TOOLS

eTOC
To subscribe
Submit an article
Recommend to your librarian
 

ARTICLE TOOLS

Publication history
Reprints
Permissions
Cite this article as

 

ORIGINAL ARTICLE   

Minerva Medica 2019 April;110(2):107-14

DOI: 10.23736/S0026-4806.18.05711-7

Copyright © 2018 EDIZIONI MINERVA MEDICA

language: English

Albiflorin inhibits the formation of THP-1-derived foam cells through the LOX-1/NF-κB pathway

Jiyou SUN 1, Xiaojuan LI 2, Kai JIAO 3, Zhiwei ZHAI 4, Dajun SUN 1

1 Department of Vascular Surgery, The Third Bethune Hospital of Jilin University, Changchun, China; 2 Department of Endocrinology, Sanmenxia Central Hospital, Sanmenxia, China; 3 Department of General Surgery, The Second Affiliated Hospital of Qiqihar Medical University, Qiqihar, China; 4 Department of General Surgery, Mudanjiang City Second People’s Hospital, Mudanjiang, China



BACKGROUND: Foam cells are characteristic pathologic cells of atherosclerosis (AS), they are lipid-loaded macrophages present on atherosclerotic lesions. A large number of studies has shown that the pathogenesis of AS is the result of interactions between the lipid metabolism disorders and chronic inflammatory responses in the body. Albiflorin can inhibit the inflammatory response and it has shown a therapeutic effect on certain inflammatory diseases.
METHODS: In this study, a human acute monocytic leukemia cell line (THP-1)-derived foam cell model was established via oxidized low-density lipoprotein (ox-LDL) to observe the effects of albiflorin on the AS-characteristic foam cells.
RESULTS: Our results showed that, after the treatment with ox-LDL, macrophages induced by propylene glycol methyl ether acetate (PMA), presented large amounts of lipid deposition in their cytoplasm, indicating that the THP-1-derived foam cell model was successfully established. On the other hand, the same cells pretreated with albiflorin presented significantly reduced amounts of lipid deposition, and their contents of total cholesterol and triglyceride were also clearly lower. Besides, the expression levels of low-density lipoprotein receptor-1 (LOX-1) and nuclear factor-κB (NF-κB) were significantly decreased, and the expression levels of downstream factors interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were also obviously decreased in the cells treated with albiflorin but not in the negative control cells. Moreover, after treatment of macrophages with different concentrations of ox-LDL, the expression levels of LOX-1 and NF-κB were up-regulated in an ox-LDL concentration-dependent manner, and so were the expression levels of IL-6 and TNF-α. And, it was found after treatment with LOX-1 neutralizing antibody or NF-κB inhibitor (during the foam cell formation induction via ox-LDL) that the lipid deposition in the cytoplasm of the cells was reduced, as in the cells treated with albiflorin.
CONCLUSIONS: Taken together, our findings suggest that albiflorin decreases lipid deposition in the cytoplasm and blocks the foaming process by regulating the LOX-1/NF-κB signaling pathway.


KEY WORDS: Albiflorin - THP-1 cells - Foam cells - NF-kappa B - Atherosclerosis

top of page