摘要目的:探讨神经激肽1受体(neurokinin 1 receptor，NK-1R)拮抗剂WIN 62，577是否对白细胞介素(interleukin，IL)-13诱导的支气管上皮细胞氧化应激损伤有保护作用。方法:培养人支气管上皮细胞(16HBE)，分为4组：对照组，IL-13组，IL-13＋SP组[IL-13＋感觉神经肽P物质(SP)]，IL-13＋WIN 62，577组。IL-13组给予IL-13(25 ng/ml)处理48 h，48 h后IL-13＋SP组给予感觉神经肽SP(10 nmol/L)处理1 h，IL-13＋WIN 62，577组给予WIN 62，577 (10 nmol/L) 处理1 h。检测各组细胞增殖活性，活性氧(reactive oxygen species，ROS)水平、丙二醛(malondialdehyde，MDA)含量及总超氧化物歧化酶(superoxide dismutase，SOD)活性。结果:与对照组比较，IL-13组细胞增殖活力减低( P<0.001)、ROS水平增高( P＝0.001)、MDA含量增高( P<0.001)、SOD活性降低( P<0.001)，差异均有统计学意义；与IL-13组比较，给予感觉神经肽SP刺激后，细胞增殖活力减低( P＝0.016)、ROS水平增高( P＝0.031)、MDA含量增高( P<0.001)、SOD活性降低( P＝0.011)；而给予WIN 62，577干预可抑制IL-13诱导的人支气管上皮细胞增殖活力降低( P＝0.018)、ROS水平增高( P＝0.018)、MDA含量增高( P<0.001)、SOD活性降低( P＝0.001)。 结论:感觉神经肽SP可加重IL-13诱导人支气管上皮细胞氧化应激损伤，NK-1R拮抗剂WIN 62，577可抑制IL-13诱导人支气管上皮细胞氧化应激损伤。

abstractsObjective:To investigate whether WIN 62, 577 which is an antagonist of neurokinin 1 receptor(NK-1R) has protective effects on interleukin(IL)-13-induced bronchial epithelial cell oxidative stress injury.Methods:Human bronchial epithelial cells (16HBE) were cultured and divided into 4 groups: control group, IL-13 group, IL-13+ SP group[IL-13+ sensory neuropeptide substance P(SP)] and IL-13+ WIN 62, 577 group.16HBE cells were treated with IL-13 (25 ng/ml) for 48 hours.After 48 hours, the IL-13 + SP group was treated with sensory neuropeptide SP(10 nmol/L) for 1 hour, and the IL-13+ WIN 62, 577 group was treated with WIN 62, 577 (10 nmol/L) for 1 hour, respectively.The proliferation ability, reactive oxygen species (ROS)level, malondialdehyde (MDA)content and total superoxide dismutase (SOD) activity in each group were detected by corresponding kits.Results:Compared with the control group, cell proliferation ability reduced ( P<0.001), ROS level increased ( P=0.001), MDA content increased( P<0.001), and SOD activity reduced ( P<0.001) in the IL-13 group.Compared with the IL-13 group, the cell proliferation ability reduced ( P=0.016), the ROS level increased ( P=0.031), the MDA content increased( P<0.001), and the SOD activity decreased ( P=0.011)after sensory neuropeptide SP stimulation.However, the intervention of WIN 62, 577 could inhibit the decrease of cell proliferation ( P=0.018), the increase of ROS level ( P=0.018), the increase of MDA content ( P<0.001), and the decrease of SOD activity ( P=0.001) in human bronchial epithelial cells induced by IL-13. Conclusion:Sensory neuropeptide SP could aggravate oxidative stress induced by IL-13 in human bronchial epithelial cells, while the sensory neuropeptide SP receptor NK-1R antagonist WIN 62, 577 could alleviate oxidative stress induced by IL-13 in human bronchial epithelial cells.