Thalidomide decreases high glucose-induced extracellular matrix protein synthesis in mesangial cells via the AMPK pathway

摘要

A previous study demonstrated the renal-protective effect of thalidomide (Thd) in diabetic nephropathy rats through the activation of the adenosine monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear factor kB (NF-icB)/monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor (TGF)-(31/mothers against decapentaplegic homolog signaling pathways. The association between AMPK inactivation and high glucose (HG)-induced meningeal cell (MC) proliferation and extracellular matrix (ECM) accumulation via NF-kB and TGF-pl signaling remains unknown. The aim of the current study was to demonstrate the effects of Thd on cell proliferation and ECM expression in HG-cultured MCs and the underlying mechanisms. HG-cultured human MCs were treated with Thd. Cell proliferation was measured by MTT assay and quantification of cell proliferation was based on the measurement of bromodeoxyuridine incorporation. The differences in TGF-pM, fibronectin and MCP-1 protein expression levels were detected via ELISA and western blot analysis.