Modulation of acute inflammation by a chitin-binding lectin from Araucaria angustifolia seeds via mast cells

Abstract

The effects of a lectin (AaL) from seeds of Araucaria angustifolia were investigated in the model of rat paw edema. In vivo anti-and pro-inflammatory activities, role of sugar residues, inflammatory mediators and systemic toxicity were assessed. Intravenous injection of AaL (0.1-1 mg/kg) dose-dependently inhibited the dextran-induced increase in edema and vascular permeability, which were prevented by association of the lectin with its binding sugar N-acetyl-glucosamine (Glyc-Nac). AaL also significantly inhibited edema induced by serotonin (18%) and compound 48/80 (33%), but not edema induced by histamine. In contrast, when applied by the s.c. route, AaL evoked a paw edema that peaked 1 h later and was partially prevented by association with Glyc-Nac (59%) or by prior i.v. administration of the lectin itself (38.8%). This AaL edematogenic activity was significantly inhibited by pentoxifylline (44.4%) or dexamethasone (51%) and also by depletion of rat paw mast cells (45.6%), but not by L-N-nitro-arginine methyl ester or indomethacin, excluding involvement of nitric oxide and prostaglandins. Treatment of animals with a single anti-inflammatory dose of AaL (1 mg/kg, i.v.) for 7 days did not affect rat corporal mass, liver, kidney, spleen or stomach wet weight, blood leukocyte count, and urea, creatinine or serum transaminase activity. Systemic toxicity was apparent only at much higher doses (LD50=88.3 mg/kg) than those required for the anti-inflammatory effect. Summarizing, AaL exerts anti-and pro-edematogenic actions via interaction with its specific lectin domain. These actions may share a common pathway involving either activation or inhibition of inflammatory mediators from resident mast cells.

Biological activities and chemical constituents of Araucaria angustifolia : An effort to recover a species threatened by extinction

“…In the carrageenan-induced peritonitis model, the pinhão lectin injected intravenously at the doses of 0.1 and 1 mg/kg inhibited neutrophil migration by 69% and 92%. Mota et al (2006) studied the effects of the lectin from A. angustifolia seeds in a rat paw edema model and observed that intravenous injection of lectin (0.1-1 mg/kg) dose-dependently inhibited the increase in vascular permeability and edema induced by dextran and serotonine. This action was due to the association of the lectin with the Nacetyl-glucosamine (Glyc-NAc) binding domain.…”

“…Thus, the pinhão lectin exerts anti-and pro-edematogenic actions by interactions with its specific domain. These actions may share a common pathway involving both the activation and inhibition of inflammatory mediators of resident mastocytes (Mota et al, 2006).…”

In vivoanti-inflammatory effect of a sulfated polysaccharide isolated from the marine brown algaeLobophora variegata

“…Paw volume was measured immediately before subcutaneous (s.c.) injection of inflammatory stimuli (0 min) into the hind paw of rats and at selected time intervals thereafter (0.5, 1, 2, 3, 4 and 5 h) by hydroplethysmometry (PanLab, LE 7500) (Mota et al, 2006). Results were expressed as increase or reduction in paw volume (mL) calculated by subtracting the basal volume measured at 0 min.…”

Chemical Constituents and Biological Activities of Araucaria angustifolia (Bertol.) O. Kuntze: A Review

“…Intravenous injection of lectin (0.01, 0.1 and 1 mg/kg) prior carrageenan reduced paw edema inhibiting the cellular event of acute inflammation via carbohydrate site interaction [59]. In another study, Mota et al [60] have described the effects of a lectin (N-acetyl-glucosamineligant) from A. angustifolia seeds in the same model of paw edema in rats, and the anti-inflammatory and pro-edematogenic actions were evaluated. Intravenous injection of lectin (0.1 and 1 mg/kg) inhibited the dextran-induced edema and vascular permeability, which were prevented by association of the lectin with its binding sugar N-acetyl-glucosamine.…”

“…Lectin also inhibited edema induced by serotonin. The mechanism associated with anti-inflammatory and pro-edematogenic actions appears to be involved in a common pathway to activation or inhibition of inflammatory mediators from resident mast cells [60].…”