Celery Seed Extract Blocks Peroxide Injury in Macrophages via Notch1/NF-κB Pathway

2015 ◽  
Vol 43 (03) ◽  
pp. 443-455 ◽  
Author(s):  
Yanhong Si ◽  
Shoudong Guo ◽  
Yongqi Fang ◽  
Shucun Qin ◽  
Furong Li ◽  
...  
Keyword(s):  
Laser Scanning ◽  
Foam Cell ◽  
Low Density Lipoprotein ◽  
Cell Formation ◽  
Density Lipoprotein ◽  
Seed Extract ◽  
Foam Cell Formation ◽  
Macrophage Foam Cell ◽  
Raw264.7 Macrophages ◽  
Celery Seed

Oxidized low-density lipoprotein (ox-LDL)-induced macrophage foam cell formation and injury is one of the major atherogenic factors. This study is aimed to investigate the protective effect of celery seed extract (CSE) on ox-LDL-induced injury of macrophages and the underlying signaling pathway. RAW264.7 macrophages were pre-incubated with CSE for 24 h, followed by stimulation with ox-LDL. Oil red O staining and enzymatic colorimetry indicated CSE significantly lessened lipid droplets and total cholesterol (TC) content in ox-LDL-injured macrophages. ELISA revealed that CSE decreased the secretion of inflammatory cytokine TNF-α and IL-6 by 12–27% and 5–15% respectively. MTT assay showed CSE promoted cell viability by 16–40%. Cell apoptosis was also analyzed by flow cytometry and laser scanning confocal microscope and the data indicated CSE inhibited ox-LDL-induced apoptosis of macrophages. Meanwhile, western blot analysis showed CSE suppressed NF-κBp65 and notch1 protein expressions stimulated by ox-LDL in macrophages. These results suggest that CSE inhibits ox-LDL-induced macrophages injury via notch1/NF-κB pathway.

Acrolein-conjugated low-density lipoprotein induces macrophage foam cell formation

2013 ◽  
Vol 227 (1) ◽  
pp. 51-57 ◽  
Author(s):  
Kenta Watanabe ◽  
Yuki Nakazato ◽  
Ryotaro Saiki ◽  
Kazuei Igarashi ◽  
Mitsukazu Kitada ◽  
...  
Keyword(s):  
Foam Cell ◽  
Low Density Lipoprotein ◽  
Cell Formation ◽  
Density Lipoprotein ◽  
Foam Cell Formation ◽  
Low Density ◽  
Macrophage Foam Cell

Abstract 442: D-4F, an Apolipoprotein A-I Mimetic Peptide, Protects Macrophages From Oxidized Low-Density Lipoprotein--Induced Apoptosis by Inhibiting the Endoplasmic Reticulum Stress-C/EBP Homologous Protein Pathway

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Shutong Yao ◽  
Hua Tian ◽  
Cheng Miao ◽  
Li Zhao ◽  
Peng Jiao ◽  
...  
Keyword(s):  
Er Stress ◽  
Foam Cell ◽  
Low Density Lipoprotein ◽  
Cell Formation ◽  
Density Lipoprotein ◽  
Foam Cell Formation ◽  
Dependent Manner ◽  
Homologous Protein ◽  
Raw264.7 Macrophages ◽  
Induced Apoptosis

Objective: D-4F, an apolipoprotein A-I (apoA-I) mimetic peptide, exerts a variety of atheroprotective functions similar to apoA-I, the major protein component of high density lipoprotein (HDL), including acting as an antioxidant, mediating cholesterol efflux from foam cells and direct anti-inflammatory effects. Our previous studies have demonstrated that endoplasmic reticulum (ER) stress promotes macrophage-derived foam cell formation by upregulating CD36 expression and mediates oxidized low-density lipoprotein (ox-LDL)-induced macrophage apoptosis. The goal of this study was to investigate the protective effect of D-4F on ox-LDL-induced macrophage cytotoxicity and specifically the ER stress-C/EBP homologous protein (CHOP) pathway-mediated apoptosis. Methods and Results: Treatment with D-4F (12.5, 25 and 50 mg/L) attenuated ox-LDL (100 mg/L)-induced cholesterol accumulation in RAW264.7 macrophages and foam cell formation in a dose-dependent manner. Similar to tunicamycin (TM), a classical ER stress inducer, ox-LDL reduced cell viability and induced apoptosis in RAW264.7 macrophages. The cytotoxic effects of ox-LDL (100 mg/L) and TM (5 mg/L) were remarkably inhibited by D-4F treatment. Interestingly, we found that D-4F also significantly suppressed the ox-LDL- and TM-induced CD36 upregulation and activation of ER stress signaling events, including the phosphorylation of inositol-requiring enzyme 1 (IRE1) and nuclear translocation of activating transcription factor 6 (ATF6). In addition, exposure of RAW264.7 macrophages to ox-LDL or TM resulted in a significant increase in the expression of CHOP, a proapoptotic transcription factor regulated by IRE1 and ATF6 under conditions of ER stress. D-4F blocked these effects in a dose-dependent manner. Moreover, administration of apoE –/– mice with D-4F (1 mg/kg per day) suppressed apoptosis and the upregulation of CD36, phospho-IRE1, GRP78 and CHOP in macrophage-dense atherosclerotic lesions. Conclusion: These data indicate that D-4F can protect macrophages from ox-LDL-induced apoptosis and that the mechanism at least partially involves its ability to inhibit the ER stress-CHOP signaling pathway.

scholarly journals Evidence of Macrophage Foam Cell Formation by Very Low-Density Lipoprotein Receptor

Circulation ◽  
2001 ◽  
Vol 103 (8) ◽  
pp. 1142-1147 ◽  
Author(s):  
Shotaro Kosaka ◽  
Sadao Takahashi ◽  
Katsuhiko Masamura ◽  
Hideo Kanehara ◽  
Juro Sakai ◽  
...  
Keyword(s):  
Foam Cell ◽  
Low Density Lipoprotein ◽  
Cell Formation ◽  
Density Lipoprotein ◽  
Foam Cell Formation ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Lipoprotein Receptor ◽  
Macrophage Foam Cell ◽  
Density Lipoprotein Receptor

scholarly journals Fluid-Phase Pinocytosis of Native Low Density Lipoprotein Promotes Murine M-CSF Differentiated Macrophage Foam Cell Formation

PLoS ONE ◽  
2013 ◽  
Vol 8 (3) ◽  
pp. e58054 ◽  
Author(s):  
Manoj K. Barthwal ◽  
Joshua J. Anzinger ◽  
Qing Xu ◽  
Thomas Bohnacker ◽  
Matthias P. Wymann ◽  
...  
Keyword(s):  
Foam Cell ◽  
Low Density Lipoprotein ◽  
Cell Formation ◽  
Density Lipoprotein ◽  
Fluid Phase ◽  
Foam Cell Formation ◽  
Low Density ◽  
Macrophage Foam Cell ◽  
Native Low Density Lipoprotein
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