异丙酚对油酸性急性肺损伤模型大鼠肺组织细胞凋亡的影响

目的:探讨静脉麻醉药异丙酚对油酸性急性肺损伤(ALI)模型大鼠肺组织细胞凋亡的影响。方法:取40只SD大鼠随机分成正常对照组、ALI组及异丙酚低、中、高剂量(4、8、16mg·kg-1·h-1)组。除正常对照组不输注油酸外,其余4组大鼠均于颈静脉输注油酸,之后各组输注相应药物4h腹主动脉放血处死,留取肺组织,光镜观察肺病理变化,流式细胞仪检测肺组织细胞凋亡率及凋亡相关蛋白Fas/FasL、Bax/Bcl-2的表达情况。结果:与正常对照组比较,ALI组肺组织细胞凋亡率显著升高(P<0.05);Bax、Fas和FasL蛋白表达均显著增强(P<0.05);Bcl-2蛋白表达显著降低(P<0.05)。与ALI组比较,异丙酚中、高剂量组肺组织细胞凋亡率、Bax、Fas和FasL蛋白表达均显著降低(P<0.05),Bcl-2蛋白表达均显著增强(P<0.05),但低剂量组上述指标变化均不显著。结论:异丙酚可能通过调控油酸性ALI时肺组织Bax/Bcl-2、Fas/FasL系统的活化而显著抑制肺组织细胞凋亡,减轻肺损伤,从而发挥一定的保护作用。

Effect of Propofoi on Apoptosis in Lung Tissue of Rats with Oleic Acidinduced Acute Lung Injury

OBJECTIVE： To investigate the effect of propofol on apoptosis in lung tissue of oleic acidinduced acute lung injury （ALI） rats. METHODS： Forty male SD rats were randomly divided into normal control group, ALI group, low, medium and high-dose （4, 8, 16 mg· kg^-1· h^-1） propofol groups. Except for the normal control group, the other 4 groups were infused with oleic acid through jugular vein followed by the infusing of the corresponding drugs for 4 h. Then the rats were sacrificed by exsanguination. Lung tissue was immediately sampled for observation of the pathologic change under light microscope and detection of apoptosis and the expression of Fas/FasL,Bax/Bcl-2 in lung tissue by FCM. RESULTS： In ALI group compared with the normal control group, the apoptosis rates in lung tissue cells was markedly increased （P 〈 0.05）; the expression of Bax, Fas and FasL in lung tissue were significantly upregulated （P 〈 0.05） while the expression of Bcl- 2 was significantly down- regulated （P〈 0.05） . Compared with ALI group, medium and high dose propofol groups significantly down- regulated the apoptosis rates and the expressions of Bax, Fas and FasL （P 〈 0.05）, significantly upregulated Bcl- 2 expression （P〈0.05） . However, there were not significant change in all above indexes in low-dose propofol group. CONCLUSIONS： It could be concluded that propofol has a protective function on ALI induced by oleic acid through inhibiting the apoptosis in lung tissue by regulating the activation of Bax/Bcl-2 and Fas/FasL systems.