Abstract
The study is aimed to determine the role of luteolin (3',4',5,7-tetrahydroxyflavone), alone and in combination with human interferon-beta (IFN-β), in modulating the immune response(s) of peripheral blood mononuclear cells (PBMCs) isolated from multiple sclerosis (MS) patients. PBMC proliferation in the presence or absence of these drugs was determined and the production of pro-inflammatory cytokines (IL-1β, TNF-α), and the ratio of cell migration mediator MMP-9, and its inhibitor, TIMP-1 was assessed in the culture supernatants. Luteolin reduced, in a dose-dependent manner, the proliferation of PBMCs, and modulated the levels of IL-1β and TNF-α released by PBMCs in the culture supernatants. Luteolin reduced the MMP-9/TIMP-1 ratio via lowering MMP-9 production. In the majority of cases, luteolin, when combined with IFN-β, had additive effects in modulating cell proliferation, IL-1β, TNF-α, MMP-9 and TIMP-1.
Highlights
Flavonoids, are group of polyphenolic compounds, known to have significant anti-tumor, antioxidant and anti-inflammatory activities [1]
At 50 μM luteolin, peripheral blood mononuclear cells (PBMCs) proliferation was reduced by 38% with no cytoxicity as indicated by trypan blue dye exclusion test
This study provides evidence that luteolin exerts beneficial immunomodulatory effect(s) on PBMCs derived from multiple sclerosis (MS) patients
Summary
Flavonoids, are group of polyphenolic compounds, known to have significant anti-tumor, antioxidant and anti-inflammatory activities [1]. 3',4',5,7-tetrahydroxyflavone, an important member of the flavonoid family has shown to exert immunomodulatory effects that may be beneficial in the treatment of neurodegenerative diseases such as multiple sclerosis (MS), which has an underlying T-cell mediated autoimmune pathology [5]. In vitro studies show that luteolin inhibits T cell activation [6] and reduces the proliferation of autoreactive T-cells induced by both alpha B-crystallin and the murine encephalitogen proteolipid protein peptide (PLP), candidate autoantigens in MS and experimental autoimmune encephalomyelitis (EAE) respectively [7]. Luteolin blocks myelin basic protein-induced mast cells' stimulation which are capable of activating T-cells [8,9]. Luteolin has been shown to reduce induction of proinflammatory cytokine from LPS-stimulated human peripheral blood mononuclear cells (PBMC) [10], LPS-stimulated dendritic cells [11] and IL-1β-activated (page number not for citation purposes)
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