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Objective To measure the expression of microRNA-646 (miR-646) in A549 cells under different concentrations of lipopolysaccharide(LPS) treatment,and to explore the possible mechanism of miR-646 in A549 cells under LPS treatment.Methods A549 cells were divided into control group and experimental groups.A549 cells from the control group were treated with RPMI-1640 and A549 cells from the experimental groups were treated with LPS (5 mg/L,10 mg/L,15 mg/L) in a duration of 24 hours.Immunocytochemical method and Western blot were used to detect the changes in surfactant protein A (SP-A) and surfactant protein C (SP-C),and quantitative real-time polymerase chain reaction was used to detect the changes in miR-646 in all groups.Results Compared with control group,the expression of SP-A in cytoplasm of A549 cells were decreased in experimental groups (all P ＜ 0.05),and LPS in different concentrations induced the expression of SP-A in A549 cells in a dose-dependent manner.Compared with control group,the expression of SP-C in cytoplasm of A549 cells was decreased in experimental groups (all P ＜ 0.05).The expression of SP-C was the lowest in 10 mg/L LPS treatment group.The relative expression level of the control group of miR-646 was 0.9597 ±0.0200,in 5 mg/L LPS treatment group it was 1.6319 + 0.1325,in 10 mg/L LPS treatment group it was 2.4762 ±0.1380,and in 15 mg/L LPS treatment group it was 1.6642 ±0.0938.There were statistically significant differences between the experimental groups and control group (all P ＜ 0.01).Conclusion miR-646 may have a biological function in acute respiratory distress syndrome through inhibiting the transcription of SP-C.
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<p><b>OBJECTIVE</b>To study long-term behavioral and ultrastructural alterations in a hypoxic-ischemic brain damage (HIBD) model of neonatal rats.</p><p><b>METHODS</b>Sixty seven-day-old Sprague-Dawley rats were randomly subjected to unilateral carotid artery ligation followed by hypoxic exposure (HIBD group) or sham operation (n=30 each). A battery of behavioral tests, including Morris water maze test and sensorimotor tests, were performed at a postnatal age of 5 weeks. Nissl staining was used for counting neurons. Transmission electron microscopy was used for observing synapse structures and measuring the thickness of the postsynaptic density area and the length of the postsynaptic active area. The correlations of histological changes with the results of behavioral tests were evaluated.</p><p><b>RESULTS</b>The HIBD group showed a significantly longer escape latency (P<0.05) and a lower frequency of original platform crossing (P<0.05) in the Morris water maze test compared with the sham operation group. The sensorimotor function test showed that the sensorimotor function in the HIBD group was worse than in the sham operation group. Nissl staining showed that the number of neurons in the HIBD group was significantly reduced (P<0.01) compared with the sham operation group. Transmission electron microscopy showed that synapses were significantly reduced in number, and that the thickness of the postsynaptic density area and the length of the postsynaptic active area were reduced in the HIBD group. The thickness of the postsynaptic density area was negatively correlated with escape latency in the Morris water maze test (r=-0.861, P<0.01), and also negatively correlated with the total score of sensorimotor function tests (r=-0.758, P<0.05) in the HIBD group.</p><p><b>CONCLUSIONS</b>Hypoxia ischemia can lead to neuron loss and ultrastructure damage, resulting in long-term deficit of behavioral functions in neonatal rats.</p>