| OBJECTIVE: Mechanical ventilation with hyperoxia is an importanttreatment to neonate respiratory distress syndrome (NRDS). However,prolonged high concentration oxygen therapy can result in lung oxygentoxicity damage, pulmonary interstitial fibrosis as well as lungdevelopmental disorders. It is also one of the main etiological factors ofbronchopulmonary dysplasia(BPD). Pulmonary inflammation and oedemais the early-specific symptom in hyperoxic lung injury.Some researchesshow that aquaporins(AQPs) is closely related with lung fluid transport,and AQPs play an important role in regulation of lung water balance. Inpresent study, we proposed to establish the rats model of hyperoxia-inducedlung injury, and observed the dynamic change regularity of AQP1 andAQP3 protein and mRNA levels in the lungs to investigate the significanceof the expressions of AQP1 and AQP3 in hyperoxia-induced lung injury. METHODS: Thirty-two juvenile(about two weeks) Wistar ratswere randomly divided into breathing room-air group (n=8) and hyperoxiaexposure group (n=8 at 3, 7 and 14days respectively). The rats in hyperoxiagroup were kept in high concentration oxygen (O2>95%) , CO2concentration ≤5%, temperature at 21℃-25℃ and humidity at 60%-70%.The room air group was kept under similar conditions in the same roomexcept 21% O2 concentration .After 3, 7, 14 days of continuous exposureto high concentration oxygen, the distribution of AQP1 and AQP3 in thelung tissues were detected by immunohistochemistry and their mRNAexpressions were measured by reverse transcription-polymerase chainreaction (RT-PCR).In addition, the ratio of lung wet weight to lung dryweight (wet-to-dry weight ratio,W/D), the protein content ofbronchoalveolar lavage fluid (BALF), lung leak index, histological changesof hyperoxia-induced lung injury were measured respectively. RESULTS:Light microscopic findings in the hyperoxia groupincluding oedema, hemorrhage and extensive inflammatory cells in thelungs were observed. In contrast, there were no such changes in theroom-air group. The lung W/D in hyperoxia group(5.21±0.24 at 3d,5.7±0.29 at 7d and 5.53±0.44 at 14d)was significantly higher than that inroom air groups(4.98±0.28), with significant differences at 7d and14d(P<0.05). The lung leak index at 3d(6.94±1.02), 7d(10.52±1.08) and14d(11.97±1.57) was much higher than that of the room-airgroup(3.35±0.46, P<0.05). The protein content in BALF at 3d(0.55±0.09),7d(0.74±0.12)and 14d(0.91±0.19)was much higher than that of theroom-air group (0.29±0.08,P<0.05). The expressions of AQP1 mRNA inthe lungs were significantly decreased in 3d of hyperoxia-exposure,minimized at 7d and increased from 14d (0.971±0.159, 0.533±0.095,0.651±0.101 respectively, vs 1.256±0.230 in room air group, P <0.05). Theexpression of AQP3 mRNA in the lung was significantly increased in 3d ofhyperoxia-exposure, maxmized at 7d and declined from 14d (0.376±0.098,0.561±0.085, 0.130±0.047 respectively, vs 0.089±0.023 in room air group,P <0.05) .The dynamic changes of AQPs protein level were coincide withthe changes of AQPs mRNA expression,and the positive regions wereAquaporin;hyperoxia;lung injury OBJECTIVE: Alveolar epithelial cell is regarded as target cell ofPulmonary inflammation, which is concerned with development and repairof injuries of lung. AT II, the stem cell of lung Alveolar epithelium,is moreimportant .Present researchs about AQPs were mainly in vivo.In this studywe detected the mRNA expression of AQP3 by semi-quantitativeRT-PCR,and expression change after H2O2 attack. METHODS: AT II(A549) cells were attacked by 60μmol/L H2O2andcollected after 12 hours culture(n=5),control group was cultured at thesame condion except H2O2 attack(n=5),The expressions of aquaporin 3 inmRNA level and their mRNA expressions after H2O2 were determinedrespectively by semi-quantitative RT-PCR. RESULTS: AQP3 mRNA expressed in A549 cell. The level of AQP3mRNA was up-regulated after H2O2 attack(0.17±0.014 vs. 0.23±0.019,n=5,P﹤0.05). CONCLUSIONS: AQP3 mRNA expressed in A549 cell. The level ofAQP3 mRNA...
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