Stimulation of Prolactin Synthesis by β- Glucan via Dectin-1 Receptors in GH3/B6 Cells

Prolactin (PRL) is a polypeptide hormone of the anterior pituitary gland that was originally named for its ability to promote lactation. In the present study, the mechanism of beta-glucan effect on GH3/B6 cells in the synthesis of prolactin has been investigated. In order to study the synthesis and secretion of prolactin, GH3 cell lines which is derived from pituitary tumors was used. Furthermore, the expressions of β-glucan dectin-1 receptors on these cells were studied. The intracellular prolactin levels were assayed by ELISA in the presence of 5, 150 and 250 μgr/ml of β-glucan for a period of 48 hours. TRH (50 nM) was used as positive control and the specific effect of beta-glucan was assessed by using dextran (150 μgr/ml). We also measured the expression of dectin-1 receptor in GH3/B6 cells. Our result showed that the higher concentrations of beta-glucan (150-250 ug/ml) significantly stimulate PRL synthesis. Most notably, for the first time we showed GH3/B6 cells express low levels of Dectin-1 receptor which greatly induced by beta glucan high concentrations. Therefore, β-glucan may induce PRL secretion throughout enhanced expression of Dectin-1 receptor.