摘要目的:探讨过氧化物酶体增殖物激活受体γ(peroxisome proliferator-activated receptor γ，PPARγ)/CD36通路在结核分枝杆菌( Mycobacterium tuberculosis， Mtb)感染巨噬细胞脂质代谢中的作用。 方法:以THP-1源性巨噬细胞建立感染模型，将实验分为对照组、 Mtb组、 Mtb+罗格列酮(rosiglitazone，ROZ)组和 Mtb+GW9662组。分别采用Western blot和RT-PCR检测巨噬细胞中PPARγ蛋白和基因表达水平；油红O染色法检测细胞内脂质情况；全自动生化分析仪检测细胞培养上清中总胆固醇(total cholesterol，TC)、甘油三酯(triglycerides，TG)、低密度脂蛋白(low density lipoprotein，LDL-C)和高密度脂蛋白(high density lipoprotein，HDL-C)浓度；免疫组织化学法检测细胞中CD36表达；CCK-8检测巨噬细胞增殖率。 结果:Mtb感染显著升高巨噬细胞中PPARγ表达( P<0.001)、促进细胞内脂质聚集及CD36表达，降低细胞培养上清中TC、TG、LDL-C和HDL-C含量( P<0.001)和细胞增殖率( P<0.001)。PPARγ激动剂ROZ可显著增强 Mtb感染所致的细胞内脂质聚集及CD36表达、进一步下调细胞培养上清中脂质水平及各细胞增殖率，而PPARγ拮抗剂GW9662则逆转上述作用。 结论:PPARγ通过影响CD36表达在 Mtb感染巨噬细胞脂质代谢中发挥一定作用。

abstractsObjective:To investigate the role of peroxisome proliferator-activated receptor γ (PPARγ)/CD36 signaling pathway in macrophage lipid metabolism after Mycobacterium tuberculosis ( Mtb) infection. Methods:THP-1-derived macrophages were infected with Mtb. Four groups were included in this study, which were control group, Mtb infection group, Mtb+ rosiglitazone (ROZ, PPARγ agonist) group and Mtb+ GW9662 (PPARγ antagonist) group. Western blot and RT-PCR were used to detect the expression of PPARγ in macrophages at protein and mRNA levels, respectively. The lipids in cells were detected by oil red O staining. The concentrations of total cholesterol (TC), triglycerides (TG), low density lipoprotein (LDL-C) and high density lipoprotein (HDL-C) in the supernatant of cell culture were detected by automatic biochemical analyzer. The expression of CD36 was detected by immunohistochemistry. CCK-8 was used to detect the proliferation rate of macrophages. Results:Mtb infection significantly increased the expression of PPARγ in macrophages ( P<0.001), promoted intracellular lipid aggregation and CD36 expression and decreased the levels of TC, TG, LDL-C and HDL-C in the supernatant of cell culture ( P<0.001) and cell proliferation rate ( P<0.001). PPARγ agonist significantly enhanced the intracellular lipid accumulation and CD36 expression that were induced by Mtb infection and down-regulated the lipid level in the supernatant of cell culture and cell proliferation rate, while PPARγ antagonist reversed the above effects. Conclusions:PPARγ played a role in lipid metabolism in Mtb-infected macrophages through affecting CD36 expression.