Premium
α‐Tocopherol counteracts ritonavir‐induced inflammatory cytokines secretion in THP‐1/macrophage cells
Author(s) -
Guo Weimin,
Meydani Mohsen,
Azzi Angelo
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1103.9
Subject(s) - ritonavir , thp1 cell line , pathogenesis , inflammation , cd36 , proinflammatory cytokine , macrophage , immunology , protease inhibitor (pharmacology) , tumor necrosis factor alpha , pharmacology , medicine , chemistry , biology , human immunodeficiency virus (hiv) , cell culture , in vitro , viral load , biochemistry , antiretroviral therapy , receptor , genetics
Treatment with protease inhibitor (PI) drugs of HIV‐infected individuals has significantly increased their life span. However, one of the side effects of PI drugs is the development of premature atherosclerosis, whose molecular pathogenesis remains unclear. Earlier, we have reported that α‐tocopherol (α‐T) normalizes CD36 overexpression and reduces oxLDL uptake in THP‐1 cells. Since inflammation is a major player in the pathogenesis of atherosclerosis, we hypothesize that PI drugs, such as ritonavir, increase pro‐inflammatory cytokines synthesis and that α‐T supplementation counteracts this effect by suppressing pro‐inflammatory cytokines synthesis. Here, we report that after differentiating THP‐1 cells to macrophages, ritonavir treatment (10μg/mL) significantly increased expression of pro‐inflammatory cytokines, IL‐6, MCP‐1 and IL‐8, both at mRNA and protein levels. This effect of ritonavir was significantly suppressed by treatment of THP‐1/macrophages with 50μM α‐T. Our data suggest that supplemental α‐T may suppress ritonavir‐induced pro‐inflammatory cytokines in HIV‐infected individuals. (Supported by USDA agreement #58‐1950‐7‐707)