Salicylate inhibits macrophage-secreted factors induced adipocyte inflammation and changes of adipokines in 3T3-L1 adipocytes.

Antidiabetic effects of salicylates have been known for years, however the cellular and molecular mechanisms of the hypoglycemic activity are not well elucidated. We examined the effects of salicylate on inflammation-related changes in gene or/and protein expressions of several adipokines in 3T3-L1 adipocytes and of LPS-induced inflammatory factors in RAW 264.7 cell. Especially, we focused our attention on the cross-talk between the macrophages and adipocytes. Exposure to RAW-CM medium resulted in an increase in the gene expression or/and protein secretion of TNF-alpha, IL-6 and resistin, and at the same time, a decrease in the gene expression of PPARgamma and adiponectin in 3T3-L1 adipocytes. Salicylate effectively reversed these changes, and up-regulated glucose consumption in adipocytes. We also found salicylate inhibited phosphorylation of NF-kappaB in RAW-CM-stimulated adipocytes. We conclude salicylate blocks inflammatory process in the pathogenesis of inflammation-related insulin resistance.