| Objective: To explore the influences of sevoflurane pretreatment on apoptosis of rat lung cells after hepatic ischemia reperfusion. Methods: Fifty-four wister rats weighing 300-350 g were randomly divided into 3 groups(n=18):sham operation group(group S, the hilum of liver was isolated but not clamped),hepatic IR group(group IR, the left and median lobe of liver was occluded for 30 min followed by reperfusion),sevoflurane preconditioning group(group SP,2.1%sevoflurane was inhaled for 30 min,and heptic IR was inducd after the end of inhalation in group SP).Six rats in each group were chosen at 30,60.and 120 min of reperfusion and sacrificed, The lung tissue was remained. Wet/dry weight ratio(W/D ratio) was determined. Colorimetry was adopted to determine activity of superoxide dismutase(SOD) and content of malondialdehyde(MDA). Terminal-deoxynucleoitidyl transferase mediated nick end labeling(TUNEL) was used to determine cell apoptosis. Cell apoptosis index(AI) was calculated. Western blot was used to determine expressions of NF-κBp65, Pathological results of lung tissue were observed under microscope. Results: W/D ratios, AIs, NF-κB activity and MDA content of group IR and group SP at each time after reperfusion were significantly increased compared with Group S((P<0.05); SOD activity was decreased significantly P<0.05); W/D ratios, AIs, NF-κB activity and MDA content of group SP were significantly lower than those of group IR((P<0.05); and SOD activity was obviously increased(P<0.05); lung tissue injury of group SP was decreased compared to group IR. Conclusions: Cell apoptosis may play an important role in lung tissue injury due to hepatic ischemia reperfusion; while sevoflurane has a certain inhibition on rat lung cell apoptosis after hepatic ischemia reperfusion. The mechanism may eliminate free radicals and inhibit lipid peroxidation by reducing activity of NF-κB in lung tissue. |
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