Investigation concerning the pathogenesis of septic condition, and development of new therapy by PPARγ activation in monocytic cells.

我们从健康志愿者身上获得巨噬细胞。分化成巨噬细胞后，脂多糖给药后在不同葡萄糖浓度的细胞培养液中培养72小时。高糖条件下巨噬细胞吞噬能力降低，内质网应激激活细胞死亡加剧。胃饥饿素通过激活过氧化物酶体增殖物激活受体（PPARγ）逆转了这些作用。

We obtained macrophage from healthy volunteers. After the differentiation into macrophage, they were cultured in different glucose concentrations of cell culture liquid for 72 hours after lipopolysaccharide administration. High glucose conditions reduced phagocytic ability and exaggerated cell death in macrophage by the activation of endoplasmic reticulum stress. Ghrelin administration reversed these effects through peroxisome proliferator-activated receptor (PPARγ) activation.