Arginase inhibition ameliorates adipose tissue inflammation in mice with diet-induced obesity.

摘要: Abstract This study examined whether oral administration of an arginase inhibitor regulates adipose tissue macrophage infiltration and inflammation in mice with high fat diet (HFD)-induced obesity. Male C57BL/6 (n = 30) were randomly assigned to control (CTL, n = 10), HFD only (n = 10), Nω-hydroxy-nor- l -arginine (HFD nor-NOHA, n = 10) groups. Plasma mRNA levels cytokines epididymal tissues (EAT), into EAT, phenotype polarization measured the animals after 12 weeks. Additionally, effects nor-NOHA on expression co-cultured 3T3-L1 adipocytes RAW 264.7 macrophages. Macrophage was significantly suppressed by treatment adipocyte/macrophage co-culture system HFD-induced Pro-inflammatory cytokines, including monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), downregulated, anti-inflammatory cytokine IL-10 upregulated nor-NOHA-treated cells. In obesity, plasma MCP-1 reduced supplementation nor-NOHA. addition, supplement modified M1/M2 ratio EAT. Oral inhibitor, altered obese tissue, thereby improved inflammatory response. These results may indicate that inhibition ameliorates obesity-induced inflammation.