| PrefaceAquaporin (AQP) is a water-selection channel molecular family, which offers fluid quickly transporting channel in life. It exists in many tissue and organs of mammal, such as brain, kidney, lung and so on. As we known, there are variety of water channel proteins expressed in lung. Among these, AQPl which mainly distributes in lung microvascular endothelial cells (LMEC) plays an important role in maintaining water balance.ObjectiveThe experiment offers theory basis and experiment evidence for deep research of lung-water metabolism disorder by observating effect of AQPl expression induced by a-Toxin in lung microvascular endothelial cell of mouse.Materials and methodsDivid 20 male Balb/c mice into test group and contrast group randomly. After supplying a-Toxin stimulation factor, divid the test group into 3 groups according to 6h,10h and 24h three time points randomly, 6h is a-Toxin 6hgroup, lOh is a-Toxin lOh group and 24h is a-Toxin 24h group, put mice to death and get samples . After giving equal NS, put the mice in contrast group to death at lOh, then get samples . Open dead mice chests, perfuse lung to wash blood off as clean as possible, prepare left lung into waxwork, which will be further stained by HE and immunohistochemistry. The immunohistochemistry stain use SP method, operate according to guide saying, via image analysis system collect images and do light density scanning semi-quantitative analysis,and checking AQP1 expression in lung microvascular endothelial cell.Statistical method adopt SPSSV11 software pack to carry out analysis of Mono-factor variance - test F of four groups and LSD of every two groups. All the results take effect when p<0.05.ResultsPathological change that due to a-Toxin groups is interstitial of lung widen, inflammatory cell infiltration and edema, alveoli structure damage . a -Toxin lOh group is the most obvious .AQP1, the immunohistochemistry stain mainly exists in LMEC, expression of AQP1 in LMEC decrease among three a -Toxin groups , a -Toxin lOh group is the most obvious.Mono-factor variance-test F of four groups is obviously different for p<0.05.LSD shows no difference between a-Toxin 6h and a-Toxin 24h the two groups for p>0.05. The other every two groups has obvious difference for p<0.05.DiscussionIt was thought that simple diffuse through gap of vessel endothelialcells or tissue epithelial cells is the way to regulate water metabolism in tissue. But these years, exploration of Aquaporin family has made people' s recognization of water metabolism mechanism produce revolutionary change.At present, 6 kinds of Aquaporin known exist in lung tissue. Among these, AQP1 mainly distributed in LMEC. It plays an important role in regulating water metabolism. One research shows permeability inter-capillary of AQP1 knocked out mice reduces 10 times than that of wild type. And AQP1 expression abundantly increases at the key time of lung fluid absorption. Lung microvascular is the important structure which forms blood-gas barrier. Among pathological course of inflammatory injury, increasing LMEC permeability is the core cycle. This research result demonstrated water permeability was direct ratio to AQP1 density, when suffered from a -Toxin stimulating, AQP1 presentation in LEMC reduced which induced water metabolism disorder. AQP1 expression increased as weaken of injury. Then resume normal. This may be one reason of lung edema happens when people suffer from injury.Conclusion1. Injecting Staphylococcus a-Toxin to mouse stomach may result in acute lung injury.2. AQP1 express on lung micro vessel endothelial cell mainly .3. AQP1 expression in LMEC decrease when lung injury is more serious. AQP1 expression increase as weaken of injury. Then resume normal steadily.
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