The Relationship And Significance Between Lung Tissue’s NIX Expression And Alveolar Cells Apoptosis After Chest Impact Injury

Traffic accident has been put in the place of “The most serious public hazard of theword” which causes threat to our daily life, while collision injury of the chest happened in thetraffic accident is said to be the second reason which usually leads to death, only ranking afterthe brain injury. Lung is the main target organ when the systemic inflammatory responsesyndrome (SIRS) is out of control. The injury will cause extensive damage to pulmonaryvascular endothelium and alveolar cell, and it shows in the form of traumatic acute lung injury(ALI), which may develop into acute respiratory distress syndrome (ARDS). The chest isVulnerable to hit, In the time when people was impacted by violence, the organs experiencesdamage, and some injuries of tissues are unavoidable, like the fracture of trachea or bronchus,lung lacerated wound, hemothorax, rib fracture, lung contusion. But these are easy todiagnose and cure. From clinical study, we know that the collision injury of chest alwaysaccompanies some injuries of other parts, and the closer of the organ located to the injuryposition, the more serious of the injury it experiences. Sometimes, the external wound willcover the visceral injury, and the second injury may happen to the organ, such as traumaticacute lung injury (ALI). The clinical features are atypical, and the treatment is easy to bedelayed for misdiagnosis and missed diagnosis.Collision injury of the lung might cause acute death of alveolar cells. Moreover, if thelung is being in the environment of long-ischemic state after the injury and it results in thesevere hypoxia of the cells leading to functional damage of mitochondria. Which of all willcause the delayed alveolar cells apoptosis. The following are the features of this kind of cellapoptosis:1) it usually happens in72hours after the injury;2) the acute alveolar cellsapoptosis relates to the original collision, while the delayed alveolar cells apoptosis is relevantto the hypoxia after the injury;3) the death mechanism of the cells is atypical apoptosis;4)after the alveolar cells apoptosis, the space is usually be filled with fibroblasts, and it will leadto pulmonary fibrosis. Therefore, lowering the delayed alveolar cells apoptosis rate after the injury is a quite important part to reduce pulmonary fibrosis and enhance the protection ofalveolar cells.By analyzing hypoxia-inducible factor which is related to the characteristics of this celldeath, NIX-being the atypical apoptosis factor of Bcl-s family, might be relevant to thedelayed alveolar cells apoptosis after ALI. Be different from other Bcl-2family member, thetime of the cells apoptosis caused by NIX is later than typical cells apoptosis, and it is similarto the characteristics of delayed alveolar cell apoptosis after the injury. NIX is induced byHIF-1to express, and by interacting with anti-apoptotic protein like Bcl-2, Bcl-X1, E1B19Kand so on, it can promote cell apoptosis.Based on the understandings above, this study builds the model of collision injury of therat chest leading to moderate and severe injury of lung, using RT-PCR, Western blot and someother molecular biological techniques to execute dynamic tests on NIX expression in lungtissue in different time after the injury; and at the same time, by observing the changes of thealveolar cells apoptosis rate with tunnel method, and exploring their relationship andsignificance, to provide experimental and theoretical basis for the prevention and treatmentof the secondary lung injury in clinical study. From this study, we can draw the followingconclusions:1．Using mini multi-functional biological impact device (BIM-Ⅲ) to impact the leftxiphoid of the rat with220Kpa pressure driven，where the apex-beat is the strongest, can buildthe steady animal heart-lung injury model. The lung injury is in moderate and severe degree,and it is in accordance with the clinical features and experimental requirements.2．This experiment shows us that NIX protein expression exists both in injury group andcontrast group in different time. NIX expression begins to increase in6h after the injury, andreaches to the peak in48h. Then it starts to decrease, and be close to the state before theinjury.3．Besides alveolar cells, NIX also shows a strong expression in vascular endothelialcells and interstitial fibrocyte.4．In24h after the injury, the lung tissue cells apoptosis mainly exists in bronchus,vascular endothelium and alveolar epithelia. The alveolar cells apoptosis rate after the injuryis obviously higher than before (p<0.01), and it reaches to the peak in72h. After that, itbegins to decrease. 5．The changes of NIX protein expression in lung tissue and the changes of alveolar cellsapoptosis rate are obviously positively correlated.Conclusion: NIX’s up-regulation involves in the pathological and physiologicalprocesses of the alveolar cells apoptosis after the injury, and its expression curve is inaccordance with the change of alveolar cells apoptosis rate. NIX might be one of the keyfactors that leads to the delayed alveolar cells apoptosis after the ALI, and this providesexperimental and theoretical basis for the future Cell and molecular mechanism research ofalveolar cells apoptosis after the injury.