Budesonide

Budesonide effectively inhibits production of eotaxin and RANTES protein although Budesonide inhibits the expression of chemokine mRNA to a variable extent in the human bronchial epithelial cell line BEAS-2B and in primary human bronchial epithelial cells. Budesonide inhibits both RANTES- and eotaxin promoter-driven reporter gene activity in the human bronchial epithelial cell line BEAS-2B and in primary human bronchial epithelial cells. Budesonide also selectively accelerates the decay of eotaxin and MCP-4 mRNA in the human bronchial epithelial cell line BEAS-2B and in primary human bronchial epithelial cells. ^[1] Budesonide time- and protein synthesis-dependently reduces VEGF secretion and VEGF mRNA expression in both cell types and these effects are inhibited by mifepristone (RU 486), a glucocorticoid receptor antagonist, suggesting that Budesonide reduces VEGF secretion and expression through its glucocorticoid receptor-mediated action. ^[2] Budesonide causes a dose-dependent, almost total, inhibition of swine dust-induced IL-6 and IL-8 release from epithelial cells and LPS-induced IL-6 and TNF-alpha from alveolar macrophages. ^[3]

Budesonide totally prevents the increased production of TNF-alpha, interleukin (IL)-1beta, IL-6, and monocyte chemoattractive protein (MCP)-1 after LPS challenge at both low (2.5 mg/mL/kg) and high (50 mg/mL/kg) concentrations in rats. ^[4] Budesonide exerts its effects of chemoprevention through growth arrest via Mad2/3 and through apoptosis via Bim/Blk and, by inference, caspase-8/9 in A/J mice. ^[5]