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

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.