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本文探讨呼吸道合胞病毒(RSV)感染人肺上皮细胞(A549细胞)后,一氧化氮(NO)的水平变化及其在RSV感染中的氧化损伤和抗病毒作用。RSV以不同时间感染A549细胞,并给予NO合成的抑制剂氨基胍(AG)处理。收集细胞培养上清,分别用硝酸还原酶法和硫代巴比妥酸法检测NO和丙二醛(MDA)含量,化学法检测羟自由基(OH·)与超氧阴离子(O2.—)水平,空斑形成试验测定病毒复制滴度(PFU)。结果显示在RSV感染4h后即上调NO、OH·、O2.—和MDA的表达水平。当RSV感染中给予AG处理以抑制iNOS合成NO时,则降低OH·、O2.—和MDA含量,但病毒PFU升高。各指标的变化与相应时间点的感染组相比,差异均有显著性。提示RSV感染肺上皮细胞诱导生成的NO与细胞内自由基水平升高和加重细胞的自由基损伤程度有关;但在一定程度上可抑制病毒的增殖水平。
This article investigates the change of nitric oxide (NO) level and its oxidative damage and antiviral activity in RSV infection after respiratory syncytial virus (RSV) infection in human lung epithelial cells (A549 cells). A549 cells were infected with RSV at different times and treated with aminoguanidine (AG), an inhibitor of NO synthesis. The cell culture supernatants were collected and the contents of NO and malondialdehyde (MDA) were detected by nitrate reductase and thiobarbituric acid respectively. The hydroxyl radical (OH ·) and superoxide anion (O2.-) Horizontal, plaque formation assay Virus replication titers (PFU) were determined. The results showed that after 4h RSV infection, the expression levels of NO, OH ·, O2.- and MDA were up-regulated. When AG treatment was given to RSV infection to inhibit NO synthesis by iNOS, OH ·, O2.- and MDA contents were decreased, but the virus PFU was increased. The change of each index compared with the corresponding time point of infection group, the difference was significant. These results suggested that the NO induced by RSV infection in lung epithelial cells was related to the increase of intracellular free radicals and the degree of free radical damage in cells. However, it could inhibit the proliferation of RSV to a certain extent.