七氟烷对急性肺损伤大鼠肺组织细胞凋亡的影响及其机制

Objective To investigate the effect and the possible mechanism of sevoflurane on lipopolysaccharide (LPS)induced acute lung injury (ALI) in rats. Methods eighteen male SD rats were randomly divided into three groups. The ALI group received LPS 5 mg/kg, while the control group received normal saline,and the sevoflurane and LPS group received sevoflurane (2.5%)for 30min after ALI induced by LPS 5 mg/kg. Lung tissue samples were taken at 12 h after instillation of LPS, histological examination by lung water contant (wet/dry ,W/D) calculation and light microcopy was performed. Apoptosis was determined by flow cytometry (FCM),TUNEL test (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) and electron microscope. At the same time, Fas, Bcl-2 protein expression were studied by using immunocytochemistry and western blot techniques in all groups mentioned above. Results The change of the levels of W/D(6.74±0.26), AI(48.1±1.9,46.6±1.2), Fas(0.223±0.034), Bcl-2(28.5±0.5) of the LPS group was significant compared with the control group (11.2±2.3,8.6±0.5,4.35±0.37,0.091±0.013,75.6±2.7), and lung injury was more severe. The levels of W/D(5.37±0.23), AI(27.2±0.9,26.3±2.4), Fas of the sevofluran group(0.131±0.21 ) were decreased, while,Bcl-2 expression (81.2±5.2) were increased compared with the LPS group (0.223±0.034,28.5±0.5)(P＜0.01), and lung injury was attenuated. Conclusion Sevoflurane inhalation protects lung from injury by inhibiting excessive cell apoptosis, Fas expression and up-regulating Bcl-2 expression, which may play an important role in the pathogenesis of LPS-induced ALI.

The mechanism of sevoflurane on the apoptosis of pulmonary cells in rats with acute lung injury induced by lipopolysaccharide