地佐辛对单肺通气后肺损伤的保护作用以及对细胞凋亡、CHOP的影响

Protective effect of dizocine on one-lung ventilation induced lung injury and its effect on apoptosis and CHOP

目的研究地佐辛对单肺通气后肺损伤的保护作用和对细胞凋亡及CCAAT/增强子结合蛋白同源蛋白(CHOP)的影响。方法选SD雄性大鼠制作大鼠单肺通气诱导肺损伤模型,随机分为双肺通气对照组(C组)、单肺通气组(O组)、低剂量地佐辛+单肺通气组(L组)和高剂量地佐辛+单肺通气组(H组),测定大鼠肺组织湿干重比(W/D),苏木精-伊红(HE)染色观察肺组织病理改变,原后末端转移酶标记(TUNEL)法检测肺组织的细胞凋亡指数(AI),蛋白质免疫印迹(Western blot)法测定肺组织GRP-78和CHOP蛋白的表达。结果与C组比较,O组大鼠W/D和AI值升高,差异有统计学意义(P<0.01);与O组比较,L组和H组大鼠W/D和AI值下降,大鼠病理生理变化减弱,差异有统计学意义(P<0.01)。与C组比较,O组大鼠GRP-78及CHOP蛋白升高,差异有统计学意义(P<0.01)。O组比较,L组和H组大鼠的GRP-78及CHOP蛋白下降,差异有统计学意义(P<0.01)。与L组比较,H组大鼠GRP-78及CHOP蛋白降低,差异有统计学意义(P<0.01)。结论地佐辛预处理对单肺通气诱导的肺损伤具有一定的保护作用,其机制与下调ERS状态下CHOP的表达,抑制细胞凋亡有关。

ObjectiveTo study the protective effect of dizocine on lung injury after single lung ventilation and its effect on apoptosis and CCAAT/enhancer binding protein homologous protein(CHOP)CHOP.MethodsSD male rats were randomly divided into two groups:control group(group C),one-lung ventilation group(group O),low-dose dizosin+one-lung ventilation group(group L)and high-dose dizosin+one-lung ventilation group(group H).The wet-dry weight ratio(W/D)of lung tissue was measured.The pathological changes of lung tissue were observed by hematoxylin-eosin staining.The cells of lung tissue were detected by TUNEL method.Apoptotic index(AI)and Western blot were used to detect the expression of GRP-78 and CHOP protein in lung tissue.ResultsCompared with control group,the W/D and AI values of group O were significantly increased(P<0.01);compared with group O,the W/D and AI values of group L and H were markedly decreased,and the pathophysiological changes of rats was remarkably decreased(P<0.01).Compared with group C,GRP-78 and CHOP protein in group O were increased significantly(P<0.01).Compared with group O,GRP-78 and CHOP protein in group L and group H were decreased significantly(P<0.01).Compared with group L,GRP-78 and CHOP protein in group H were significantly lower(P<0.01).ConclusionDizosin pretreatment has a protective effect on lung injury induced by one-lung ventilation,and its working mechanism may be through the down-regulation of CHOP expression in ERS state and inhibition of apoptosis.