高浓度氧对未成年大鼠肺部炎症反应的影响

目的 探讨高浓度氧对未成年大鼠肺部炎症反应的影响.方法 将40只出生21 d的SD大鼠按随机数字表法分为空气对照组及高氧暴露12、24、48、72 h组,每组8只,分别将大鼠置于空气和常压高氧箱(氧含量达92%～94%)中.于相应时间点采用放血法处死大鼠后取肺组织,并行支气管肺泡灌洗.采用硫代巴比妥酸法和比色法分别测定肺组织丙二醛(MDA)含量及髓过氧化物酶(MPO)活性;采用酶联免疫吸附法(ELISA)检测支气管肺泡灌洗液(BALF)中肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和IL-10含量;观察肺组织病理改变,并进行肺损伤评分.结果 与空气对照组比较,高氧暴露12 h肺组织MDA含量(mmol/g)即显著升高(2.24±0.43比1.57±0.31),MPO活性(U/g)于高氧暴露24 h显著升高(1.24±0.25比0.69±0.22),并均随高氧暴露时间延长逐渐增加(P<0.05或P<0.01).BALF中TNF-α、IL-6和IL-10含量于高氧暴露24 h时较空气对照组显著增加[TNF-α(ng/L):135.2±44.0比94.5±22.3,IL-6(ng/L):73.1±14.2比55.7±17.3,IL-10(ng/L):67.9±21.7比48.2±7.6,P<0.05或P<0.01];但高氧暴露48 h时较24 h时显著降低(48 h时BALF中TNF-α、IL-6、IL-10分别为105.4±17.0,54.3±17.4,50.9±6.9,均P<0.05).高氧暴露12 h时肺损伤评分(分)即较空气对照组显著升高(4.5±1.4比1.3±0.5),并随高氧暴露时间延长进一步升高(P<0.05或P<0.01).结论 高浓度氧可引起未成年大鼠肺部炎症损伤;炎症细胞因子的出现高峰均在高氧暴露24 h.

Effects of hyperoxia on inflammatory response in lung of infantile rats

Objective To investigate the effects of hyperoxia on inflammatory response in lung of infantile rats. Methods Forty 21-day-old male Sprague-Dawley (SD) rats were randomly divided into five groups: room-air control group and 12, 24, 48, 72 hours hyperoxia groups, with the rats continuously exposed to room-air and oxygen (92%-94%) respectively. The rats were sacrificed by depletion method, and lung tissue was obtained for bronchoalveolar lavage. The contents of malondialdehyde (MDA) and the activities of myeloperoxidase (MPO) in lung tissue were assayed by thiobarbituric acid or chromometry, and the concentrations of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-10 in bronchoalveolar lavage fluid (BALF) were measured by enzyme linked immunosorbent assay (ELISA). The lung pathology was examined, and lung injury score was assessed. Results Compared with the room-air control group, the contents of MDA [(2.24±0.43) mmol/g vs. (1.57±0.31) mmol/g] and the activities of MPO [(1.24±0.25) U/g vs. (0.69±0.22) U/g] from lung tissue were elevated at 12 hours and 24 hours of hyperoxia exposure, respectively, and they further increased with prolongation of hyperoxia exposure (P<0.05 or P<0.01). The values of TNF-α [(135.2±44.0) ng/L vs. (94.5±22.3) ng/L], IL-6 [(73.1±14.2) ng/L vs. (55.7±17.3) ng/L] and IL-10 [(67.9±21.7) ng/L vs. (48.2±7.6) ng/L] in BALF were all higher at 24 hours of hyperoxia exposure than those of the room-air control group (P<0.05 or P<0.01), but decreased at 48 hours of hyperoxia exposure compared with those of 24-hour hyperoxia exposure group [TNF-α: (105.4±17.0) ng/L, IL-6: (54.3±17.4) ng/L, IL-10: (50.9±6.9) ng/L, all P<0.05]. Lung injury scores were higher at 12 hours of hyperoxia exposure as compared with those of the room-air control group (4.5±1.4 vs. 1.3±0.5), and it further increased with prolongation of hyperoxia exposure (P<0.05 or P<0.01). Conclusion Hyperoxia can lead to lung inflammatory injury in infantile rats, and the expressions of TNF-α, IL-6 and IL-10 in BALF may reach the peak at 24 hours of hyperoxia exposure.