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Inflammation. 2014 Dec;37(6):2020-9. doi: 10.1007/s10753-014-9934-x.

Inhibition of macrophage migration inhibitory factor reduces diabetic nephropathy in type II diabetes mice.

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School of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.


Macrophage migration inhibitory factor (MIF) plays a critical role in inflammation and is elevated in diabetic kidney. However, whether MIF plays a causative role in diabetic nephropathy (DN) remains unclear. In the present study, we have demonstrated that after treatment of 8-week-old diabetic db/db and nondiabetic db/m mice with the MIF inhibitor ISO-1 (20 mg/kg) for 8 weeks, there was a significant decrease in blood glucose, albuminuria, extracellular matrix accumulation, epithelial-mesenchymal transition (EMT), and macrophage activation in the kidney of db/db mice. Incubation of macrophages with MIF induced the production of proinflammatory cytokines, including interleukin (IL) 6, IL-1β, tumor necrosis factor α (TNF-α). The conditioned media (CM) of MIF-activated macrophages and TNF-α induced by MIF caused podocyte damage. Moreover, CM from MIF-activated macrophages induced EMT of renal tubular cells, and this effect was blocked by ISO-1. Thus, MIF inhibition may be a potential therapeutic strategy for DN. This effect may be attributable to its inhibitory effect on macrophage activation in the diabetic kidney.

[Indexed for MEDLINE]

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