Section of Preventive and Public Health Dentistry, Division of Oral Health, Growth and Development, Faculty of Dental Science, Kyushu University, Fukuoka, Japan.
Free Radic Res. 2011 Mar;45(3):336-41. doi: 10.3109/10715762.2010.532495. Epub 2010 Nov 1.
It has previously been reported that the globular form of adiponectin (gAd), mature adipocyte-derived cytokine, induced generation of reactive oxygen species (ROS) and nitric oxide (NO) in the murine macrophage cell line RAW 264. This study investigated whether diacylglycerol kinases (DGKs), enzymes functioning in sub-cellular signalling pathways, had a role on gAd-induced ROS generation in RAW 264 cells. Administration of R59022, a specific inhibitor for DGK, reduced gAd-induced ROS generation and NO release. RAW 264 cell expressed DGKα mRNA. Depression of DGKα mRNA by RNA interference significantly reduced the ROS generation in response to gAd treatment. Interestingly, transfection with the DGKα-specific small interfering RNA attenuated the expression level of Nox1 mRNA in gAd-treated RAW 264 cells. In addition, the DGKα knockdown with siRNA suppressed gAd-induced NO release.
先前有报道称，球状形式的脂联素（gAd），成熟脂肪细胞来源的细胞因子，可诱导鼠源巨噬细胞系 RAW 264 中活性氧（ROS）和一氧化氮（NO）的产生。本研究探讨了二酰基甘油激酶（DGK），在细胞内信号通路中起作用的酶，在 RAW 264 细胞的 gAd 诱导 ROS 产生中是否有作用。R59022，一种 DGK 的特异性抑制剂，可减少 gAd 诱导的 ROS 生成和 NO 释放。RAW 264 细胞表达 DGKα mRNA。用 RNA 干扰使 DGKα mRNA 下调可显著减少 gAd 处理时 ROS 的产生。有趣的是，用 DGKα 特异性小干扰 RNA 转染可减弱 gAd 处理的 RAW 264 细胞中 Nox1 mRNA 的表达水平。此外，用 siRNA 抑制 DGKα 可抑制 gAd 诱导的 NO 释放。
