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Acute effect of β-sitosterol on calcium uptake mediates anti-inflammatory effect in murine activated neutrophils

Authors


Tânia Silvia Fröde, Department of Clinical Analysis, Centre of Health Sciences, Federal University of Santa Catarina, Campus Universitário – Trindade, Florianópolis 88040-970, SC, Brazil. E-mail: saleh@ccs.ufsc.br

Abstract

Objectives  To evaluate the effect of β-sitosterol on 45Ca2+ uptake in activated murine neutrophils, and upon myeloperoxidase and adenosine deaminase activity, and interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α) levels, in carrageenan-induced inflammation in the mouse air pouch model.

Methods  Dried Esenbeckia leiocarpa bark was macerated and extracted resulting in a crude hydroalcoholic extract (CHE) that was partitioned to obtain an alkaloid fraction. The alkaloid was then partitioned in polar and nonpolar subfractions. β-Sitosterol was isolated from the nonpolar subfraction and identified by comparison with the literature. The effect of β-sitosterol on 45Ca2+ uptake in activated murine neutrophils, and upon myeloperoxidase and adenosine deaminase activity, IL-1β and TNF-α levels in carrageenan-induced inflammation in mice were evaluated.

Key findings  β-Sitosterol promoted a time- and dose-dependent increase of the calcium uptake in activated neutrophils that was promptly reversed by nifedipine, BAPTA-AM, LY294002, and colchicine. β-Sitosterol inhibited myeloperoxidase and adenosine deaminase activity, and IL-1β and TNF-α levels.

Conclusions  β-Sitosterol inhibited either myeloperoxidase and adenosine deaminase activity or IL-1β and TNF-α levels. This effect seemed to be mediated by the calcium uptake in activated neutrophils in a time- and concentration-dependent manner through L-type voltage dependent calcium channels, intracellular calcium, phosphoinositide kinase-3, and microtubule modulation.

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