丙泊酚预先给药对急性肺损伤大鼠自噬相关蛋白Beclin-1表达的影响

Effect of propofol pretreatment on the expression of Beclin-1 in rats with acute lung injury

目的 探讨丙泊酚预先给药对脂多糖（LPS）所致急性肺损伤的影响及其机制.方法 将45只雄性SD大鼠随机分为3组：对照组（C组）、LPS组（L组）和LPS＋丙泊酚组（LP组）,每组15只.C组尾静脉注射生理盐水;L组尾静脉注射LPS 7.5 mg/kg;LP组在尾静脉注射LPS7.5 mg/kg的基础上加用丙泊酚30 mg/kg.实验结束后放血处死大鼠,取肺组织进行病理学检查并测定肺湿/干重比（W/D）;计算肺湿/干比重比值（W/D比值）、MPO活性及肺泡灌洗液中总蛋白含量,光镜下行WBC计数,同时Western blot检测肺组织中Beclin-1表达.结果 与C组比较,L组肺组织中W/D比值、WBC计数及总蛋白含量[5.21±0.27、（6.57 ±1.25）×10^6/L、（2.01±0.32）g/ml]均明显升高（P＜0.05）,Beclin-1蛋白的表达水平（0.31 ±0.11）明显升高;与L组比较,W/D比值、WBC计数及总蛋白含量[4.41 ±0.21、（2.67±0.38）×10^6/L、（0.27 ±0.11） g/ml]明显降低（P＜0.05）,Beclin-1蛋白的表达水平（0.47 ±0.15）亦明显升高.结论 丙泊酚具有肺保护作用,且该作用可能与其增加细胞内自噬相关基因Beclin-1表达有关.

Objective To investigate the protective effect of propofol pretreatment in a rat model of acute lung injury and the possible mechanisms. Methods Forty-five male SD rats weighing [ （250- 280） g] were randomly divided into 3 groups （n = 15 each） ： control group （group C）, lipopolysaccharide （LPS） group （group L） and LPS ＋ propofol group （group LP）. Saline solution was injected into rats of group C through caudal vein. LPS （7.5 mg/kg） was injected into rats of group LP through caudal vein. LPS （7.5 mg/kg） and propofol （30 mg/kg） were injected into the rats of group LP through caudal vein at the same time. After the experiment, the lung wet-to-dry weight ratio （ W/D ） , total protein （TP） con- tents, and counts of white blood cells （WBC） in broncho-alveolar lavage fluid （BALF） were determined. The expression of Becinl was measured by Western blotting. Results As compared with group C, the W/D, WBC counts, TP contents and expression of Beclin-1 were significantly increased in group L [5.21 ±0. 27, （6. 57 ± 1.25） × 10^6/L, （2. 01 ± 0. 32） g/ml and 0. 31 ± 0. 11 respectively）. As compared with group L, the W/D, WBC counts, TP contents and expression of Beclin-1 were significantly increased in group L [4.41 ±0. 21, （2. 67±0. 38）× 10^6/L, （0. 27 ±0. 11 ） g/ml and 0. 47 ±0. 15 respectively ]. Conclusion Propotol exerts a lung protective effect in the rats of ALl, which may be associated with the expression of autophagy related protein Beclin-1.