Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
Inflammation. 2015 Feb;38(1):415-23. doi: 10.1007/s10753-014-0046-4.
Propofol is a widely used intravenous anesthetic. The aim of this study was to investigate the roles of nuclear factor erythroid-2-related factor 2 (Nrf2) and NADPH oxidase (NOX) in propofol protection in inflammatory conditions induced by lipopolysaccharide (LPS). Human alveolar epithelial cells (A549 cell line) were incubated with propofol (10, 25, and 50 μmol/L) for 1 h and then treated with LPS (100 ng/mL) for 24 h. Results indicated that propofol not only attenuated LPS-induced expression of iNOS, NOX, and COX2, but decreased the production of ROS, NO, and PGE2 as well. Propofol also increased the GSH levels and the mRNA and protein levels of Nrf2. Notably, Nrf2 siRNA and the inhibitors of COX-2 and NOX attenuated the inhibition of propofol on ROS production. In conclusion, propofol reduced LPS-induced ROS production via inhibition of inflammatory factors and enhancement of Nrf2-related antioxidant defense, providing its cytoprotective evidence under inflammatory conditions.
异丙酚是一种广泛应用的静脉麻醉剂。本研究旨在探讨核因子红细胞 2 相关因子 2（Nrf2）和 NADPH 氧化酶（NOX）在脂多糖（LPS）诱导的炎症条件下异丙酚保护中的作用。将人肺泡上皮细胞（A549 细胞系）用异丙酚（10、25 和 50μmol/L）孵育 1 小时，然后用 LPS（100ng/mL）处理 24 小时。结果表明，异丙酚不仅减弱了 LPS 诱导的 iNOS、NOX 和 COX2 的表达，还降低了 ROS、NO 和 PGE2 的产生。异丙酚还增加了 GSH 水平以及 Nrf2 的 mRNA 和蛋白水平。值得注意的是，Nrf2 siRNA 和 COX-2 和 NOX 的抑制剂减弱了异丙酚对 ROS 产生的抑制作用。总之，异丙酚通过抑制炎症因子和增强 Nrf2 相关抗氧化防御来减少 LPS 诱导的 ROS 产生，为其在炎症条件下的细胞保护提供了证据。
