Naringin possesses strong antioxidative activity and can protect against some respiratory diseases. Oxidative stress is thought to be a major factor in the development of many tobacco-caused diseases. The nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway plays a critical role in the regulation of oxidative stress. The dynamic changes in the antioxidant system in the lung that are induced by cigarette smoke (CS) are not well investigated, and how naringin affects these changes remains unknown. This study aimed to investigate the dynamic changes between the oxidation and antioxidant systems resulting from CS exposure and the effects of naringin on these changes in mice. Mice were chronically exposed to CS for 30 days. The levels of malondialdehyde (MDA), glutathione (GSH), interleukin (IL)-6, and tumor necrosis factor-alpha (TNF-α); the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px); and the expressions of Nrf2, heme oxygenase-1 (HO-1), and nicotinamide adenine dinucleotide phosphate quinone dehydrogenase 1 (NQO1) in lung tissue were measured on days 2, 7, and 30. The levels of MDA, GSH, IL-6, and TNF-α in the lung were found to increase throughout the exposure. SOD and GSH-Px activities showed an increase on day 2 and a decrease on days 7 and 30. The messenger ribonucleic acid expressions of Nrf2, HO-1, and NQO1 were elevated on day 2 and decreased on day 7; Nrf2 and HO-1 expressions were continually decreased, but NQO1 expression was increased again, on day 30. Naringin restored the levels of these biochemical indices to normal throughout the experiment, suggesting that naringin protected against the CS-induced oxidative damage by suppressing the increase of antioxidants resulting from the early stage of CS exposure, as well as inhibiting the depletion of antioxidants due to long-term oxidative stress. Naringin also suppressed lung inflammation by inhibiting IL-6 and TNF-α. These results indicate that naringin possesses a powerful ability to maintain the balance of the oxidation/antioxidant system in the lung when subjected to CS exposure, probably by regulating the Nrf2 signaling pathway.

柚皮苷具有很强的抗氧化活性，可以预防某些呼吸系统疾病。氧化应激被认为是许多烟草引起的疾病发展的主要因素。核因子红系2相关因子2（Nrf2）信号通路在氧化应激的调节中起关键作用。香烟烟雾（CS）引起的肺部抗氧化系统的动态变化尚未得到很好的研究，而柚皮苷如何影响这些变化仍然未知。这项研究旨在调查CS暴露引起的氧化和抗氧化系统之间的动态变化以及柚皮苷对小鼠这些变化的影响。将小鼠长期暴露于CS 30天。丙二醛（MDA），谷胱甘肽（GSH），白介素（IL）-6，和肿瘤坏死因子-α（TNF-α）；超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）的活性；在第2、7和30天测量肺组织中Nrf2，血红素加氧酶-1（HO-1）和烟酰胺腺嘌呤二核苷酸磷酸醌醌脱氢酶1（NQO1）的表达。MDA，GSH，IL-如图6所示，在整个暴露过程中发现肺中的TNF-α升高。SOD和GSH-Px活性在第2天增加，在第7天和第30天减少。Nrf2，HO-1和NQO1的信使核糖核酸表达在第2天升高，在第7天降低。在第30天，Nrf2和HO-1的表达持续降低，但NQO1的表达再次升高。柚皮苷在整个实验过程中将这些生化指标的水平恢复到正常水平，提示柚皮苷可通过抑制CS暴露早期引起的抗氧化剂的增加，并抑制由于长期氧化应激引起的抗氧化剂的消耗，从而防止CS引起的氧化损伤。柚皮苷还通过抑制IL-6和TNF-α抑制肺部炎症。这些结果表明，柚皮苷具有很强的能力，可以通过调节Nrf2信号通路来维持CS暴露时维持肺中氧化/抗氧化系统的平衡。