Abstract
Isoflavonoids have been largely studied due to their distinct biological activities identified thus far. Herein, we evaluated the activity of neovestitol, an isoflavonoid isolated from Brazilian red propolis, in acute and chronic inflammation. As for acute inflammation, we found that neovestitol reduced neutrophil migration, leukocyte rolling and adhesion, as well as expression of ICAM-1 in the mesenteric microcirculation during lipopolysaccharide-induced acute peritonitis. No changes were observed in the levels of TNF-α, CXCL1/KC and CXCL2/MIP-2 upon pretreatment with neovestitol. The administration of an inducible nitric oxide synthase (iNOS) inhibitor abolished the inhibitory effects of neovestitol in neutrophil migration and ICAM-1 expression. Nitrite levels increased upon treatment with neovestitol. No effects of neovestitol were observed on the chemotaxis of neutrophils in vitro. As for chronic inflammation, neovestitol also reduced the clinical score and joint damage in a collagen-induced arthritis model. There was no change in the frequency of IL-17-producing TCD4+ cells. In addition, pretreatment with neovestitol reduced the levels of IL-6. These results demonstrate a potential anti-inflammatory activity of neovestitol, which may be useful for therapeutic purposes and/or as a nutraceutical.
Highlights
Isoflavonoids have been largely studied due to their distinct biological activities identified far
We found that intraperitoneal injection of LPS induced significant neutrophil migration into the peritoneal cavity of mice as compared with the group that did not receive the LPS challenge (Veh) (Fig. 1A)
We investigated the activity of neovestitol on leukocyte rolling and adhesion and on intercellular adhesion molecule type 1 (ICAM-1) expression in mesenteric microcirculation of LPS-challenged mice
Summary
Isoflavonoids have been largely studied due to their distinct biological activities identified far. The inflammatory process comprises a set of events involving the participation of cytokines (TNF-α), chemokines (CXCL1/KC and CXCL2/MIP-2), lipid mediators (leukotriene B4), cell adhesion molecules (ICAM-1), nitric oxide and immune cells. This process leads to vasodilation, increased vascular permeability and leukocyte recruitment[1]. Chronic inflammation is a persistent phenomenon in which the presence of macrophages and lymphocytes becomes more evident[2] It is a host protective response, exacerbation of inflammation in some cases is directly related to tissue damage, requiring the use of anti-inflammatory drugs[3].
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