Effects Of Propofol On Apoptosis Of Alveolar Cell In Ischemia-reperfusion Injury And Expression Of Fas, Bcl-2 In Rat Lung

Objective To evaluate the effects of propofol of the dynamic changes of alveolar apoptosis in ischemia-reperfusion injury in rat lungMethods 96 male rats were randomly divided into 4 groups:Group A: control group(n=6, species were taken directly after anesthesia and thoracic incision.This group served as the pre-operative controls to the other groups),Group B: Sham group(n=30,suture was only placed in right hilus.The other operation progress and analysis of species were same to IR group),Group C: Ischemia-reperfusion group(n=30,according to time,It is further divided into 5 sub-groups stands for before deligation,30min after ischemis,1h,2h,4h after reperfusion),Group D:propofol treatment group(n=30, five sub-groups as group C). We use the rat model of warm ischemia and repefusion in situ in single lung. The alveolar apoptosis index was achieved by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL). The expression of Fas,Bcl-2 in lung tissue was accessed by quantitative immunohistochemistry. And meanwhile,Pa02,wet/dry ratio of lung tissue were recorded,indicating the dynamic progress of pulmonary function deterioration in ischemia-reperfusion injury.Morphological and ultrastructural changes of lung tissue was observed by either light microscopy or transmission electron microscopy. Results Compared with shame group,Ischemia-reperfusion group showed decreased Pa02 and elevated wet/dry ratio.Apoptotic index was elevated with a prominent elevation of expression of Fas in lung(P<0.05). Compared with Ischemia-reperfusion group,propofol treatment group showed elevated Pa02 and decreased wet/dry ratio.Apoptotic index was decreased with a prominent decrease of expression of Fas and elevation ofexpression of Bcl-2 in lung(P<0.05).Conclusions Propofol can ameliorate pulmonary IR injury and inhibit alveolar apoptosis,one important role may be it is down-regulation on Fas expression and up-regulation on bcl-2 expression in lung.