PPARg Deficiency Suppresses the Release of IL-1b and a in Macrophages via a Type 1 Interferon Dependent Mechanism

TG elicited Peritoneal macrophages from WT and PPARgamma KO mice were treated with control or lipid inflammatory stress in triplicate LysM-Cre (cre) controls) or LysM-PPARg (ppar) were treated with vehicle (BSA-PBS; bp) or palmitate (250 uM) with LPS (100 ng/ml); pl for 8h and RNA was extracted

本实验中，取自野生型（WT）与过氧化物酶体增殖物激活受体γ基因敲除（PPARgamma KO）小鼠的TG诱导型腹腔巨噬细胞，以对照条件或脂质炎性应激条件进行处理，每组设置三次生物学重复。此外，LysM-Cre（cre）对照细胞与LysM-PPARg（ppar）细胞分别采用溶剂对照（BSA-PBS；bp）、250μM棕榈酸联合100ng/ml脂多糖（LPS）处理，孵育8小时后提取总RNA。