Metaproterenol (10 μM; 74 hours; THP-1 cells and bone marrow macrophages) treatment causes downregulation of NF-κB in high glucose-induced THP-1 cells and bone marrow macrophages. Metaproterenol (10 μM; 74 hours; THP-1 cells and bone marrow macrophages) treatment increases β-arrestin2 and its interaction with IκBα in high glucose-induced THP-1 cells and bone marrow macrophages [1].

Metaproterenol (Zucker diabetic fatty rats; 12 weeks ) treatment, decreases monocyte activation as well as pro-inflammatory and pro-fibrotic responses in the kidneys and heart. Metaproterenol might have protective effects against diabetic renal and cardiovascular complications[1].