Abstract
BackgroundDietary flavonols may play an important role in the adjunct therapy of chronic inflammation. The availability of therapeutic formulations of pentahydroxyflavone glycoside, rutoside (RU), led us to investigate the ability of this molecule to modulate the release of various proinflammatory mediators from human activated macrophages in vitro and to ameliorate arthritic markers in a rat model.MethodsRU was added simultaneously to human macrophages during their activation. Cells were then analyzed for inflammation-related gene expression using a specific array, and cell supernatants were collected to measure inflammatory mediators. RU was also injected into adjuvant-induced arthritic rats, and disease progression and body weight were evaluated until 50 days after injection. Sera and peritoneal macrophages were also collected to quantify the RU effect on various inflammatory markers.ResultsRU inhibited inflammation-related gene expression in activated human macrophages and the release of nitric oxide, tumor necrosis factor-alpha, interleukin (IL)-1, and IL-6 from these cells. In a rat model, RU inhibited clinical signs of chronic arthritis, correlating with decreased levels of inflammatory cytokines detected in rat sera and macrophage supernatants.ConclusionThus, RU may have clinical value in reducing inflammatory manifestations in human arthritis and other inflammatory diseases.
Highlights
The immune system has evolved to protect the host from microbial infection
RU inhibited clinical signs of chronic arthritis, correlating with decreased levels of inflammatory cytokines detected in rat sera and macrophage supernatants
Inhibition of gene transcription in human macrophage by rutoside In vitro, RU has generally been shown to display its activities at concentrations of 30 to 200 μM [19]
Summary
The immune system has evolved to protect the host from microbial infection. a breakdown in the immune system often results in infection, cancer, and autoimmune diseases. Rheumatoid arthritis (RA), type 1 diabetes, inflammatory bowel disease, myocarditis, thyroiditis, uveitis, systemic lupus erythromatosis, and myasthenia gravis are organ-specific autoimmune diseases that afflict more than 5% of the population worldwide Their etiology is not known and a cure is still wanting, promising data raised in human RA implied macrophage mediators in disease progression [1,2]. During RA, patients have an increased number of monocytes, inflammatory monocytes, circulating in peripheral blood [4,5,6] and have an elevated number of macrophages in the joints [5] These cells are highly activated and are one of the main producers of interleukin (IL)-1β and tumor necrosis factor-alpha (TNF-α), two essential proinflammatory cytokines required for the pro-. The availability of therapeutic formulations of pentahydroxyflavone glycoside, rutoside (RU), led us to investigate the ability of this molecule to modulate the release of various proinflammatory mediators from human activated macrophages in vitro and to ameliorate arthritic markers in a rat model
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