Luo Jinhua, Sun Jia, Cai Dehong
Department of Endocrinology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.E-mail:
Nan Fang Yi Ke Da Xue Xue Bao. 2014 Jun;34(6):787-91.
To investigate the role of Toll-like receptor 4 (TLR4) signaling pathway in the activation of rennin- angiotensin system (RAS) in adipose cells.
3T3-L1 cells induced with isobutylmethylxanthine, insulin and dexamethasone to differentiate into adipocytes were stimulated by LPS with or without irbesartan pretreatment. The expression levels of TLR4, angiotensinogen (AGT) and angiotensin II receptor type 1 (ATlR) mRNA in 3T3-L1 cells was determined by RT-PCR, and their protein expressions were detected with Western-blotting. Immunofluorescence double staining was used to observe the translocation of NF-κB p65 subunit in the cells.
Stimulation with LPS dose- and time-dependently increased the mRNA and protein expressions of TLR4, AGT and AT1R. LPS exposure resulted in enhanced translocation of NF-κB p65 subunit in the adipose cells, which was attenuated by irbesartan pretreatment.
Activation of TLR4 signaling pathway may trigger the activation of local RAS in adipose cells.
探讨Toll样受体4（TLR4）信号通路在脂肪细胞肾素-血管紧张素系统（RAS）激活中的作用。
用异丁基甲基黄嘌呤、胰岛素和地塞米松诱导3T3-L1细胞分化为脂肪细胞，在有或无厄贝沙坦预处理的情况下用脂多糖（LPS）刺激。通过逆转录聚合酶链反应（RT-PCR）测定3T3-L1细胞中TLR4、血管紧张素原（AGT）和血管紧张素II 1型受体（AT1R）mRNA的表达水平，并用蛋白质免疫印迹法检测其蛋白表达。采用免疫荧光双染色观察细胞中核因子κB p65亚基的转位情况。
LPS刺激剂量和时间依赖性地增加了TLR4、AGT和AT1R的mRNA和蛋白表达。LPS暴露导致脂肪细胞中核因子κB p65亚基的转位增强，而厄贝沙坦预处理可使其减弱。
TLR4信号通路的激活可能触发脂肪细胞中局部RAS的激活。
