南方医科大学学报

南方医科大学学报 ›› 2013, Vol. 33 ›› Issue (04): 469-.

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Effects of sevoflurane on pulmonary cytosolic phospholipase A2 and clara cell secretory protein expressions in rabbits with one-lung ventilation-induced lung injury

刘睿，杨泳，李艳华，李江，马庆杰，赵艳花，王殿华   

  • 出版日期:2013-04-20 发布日期:2013-04-20

  • Online:2013-04-20 Published:2013-04-20

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摘要： 目的探讨七氟醚对单肺通气（OLV）兔肺组织胞质型磷脂酶A2（C-PLA2）及clara细胞分泌蛋白（CCSP）表达的影响。方
法36只健康日本大耳白兔随机分为假手术组（S组）、OLV组（O组）和OLV+七氟醚组（OS组）。OS组据所给七氟醚浓度（体积
分数）不同分为1%、2%、3%和4%亚组。Western blotting和定量PCR分别用于检测肺组织中CCSP和C-PLA2蛋白及mRNA的
表达水平。ELISA检测肺组织花生四烯酸（AA）含量。通过观察肺湿/干（W/D）和肺组织的形态学改变评价肺损伤的严重程
度。结果OLV后兔肺组织CCSP蛋白和mRNA表达水平明显降低（P<0.05），而C-PLA2蛋白和mRNA表达水平、肺组织AA含
量和肺损伤程度均明显增加（P<0.05）；OLV+七氟醚组中肺组织CCSP 蛋白和mRNA表达增加（P<0.05），而C-PLA2蛋白和
mRNA表达水平和肺组织AA含量降低（P<0.05），肺损伤减轻（P<0.05）；OLV+不同浓度七氟醚组中肺组织CCSP蛋白和mRNA
表达水平无显著性差异，但肺组织C-PLA2蛋白和mRNA表达水平、肺组织AA含量和肺损伤程度随浓度的增加而逐渐降低（P<
0.05）。结论OLV可使兔肺组织中CCSP蛋白和mRNA表达水平降低，肺组织C-PLA2蛋白和mRNA表达水平和AA含量增加，
引起急性肺损伤。七氟醚可通过逆转OLV的上述效应而发挥抗急性肺损伤作用。

Abstract: Objective To investigate the effects of sevoflurane on cytosolic phospholipase A2 (C-PLA2) and clara cell secretory
protein (CCSP) in lung tissues of rabbits with one-lung ventilation (OLV)-induced lung injuries. Methods Thirty-six healthy
Japanese white rabbits were randomized into sham-operated group, OLV group, and OLV plus sevoflurane group subdivided
into 4 subgroups with sevoflurane concentrations of 1%, 2%, 3% and 4%. CCSP and C-PLA2 mRNA and protein expressions in
rabbit lung tissues were detected by Western blotting and real-time PCR, and the content of arachidonic acid (AA) was
measured using ELISA. The severities of the lung injury were evaluated according to lung wet/dry weight (W/D) ratio and
histological scores. Results In the OLV group and OLV+ sevoflurane groups, pulmonary CCSP expressions were significantly
lower, while C-PLA2 expression, lung W/D ratios and lung histological scores were significantly higher than those in the
sham-operated group (P<0.05). Compared with OLV group, the OLV + sevoflurane groups showed significantly increased
expressions of CCSP and reduced C-PLA2 expression, lung W/D ratios and histological scores (P<0.05). In the 4 OLV +
sevoflurane groups, CCSP expressions underwent no significant changes as sevoflurane concentration increased, but C-PLA2
expressions, lung W/D ratios and histological scores all decreased gradually as the concentrations of sevoflurane increased (P<
0.05). Conclusion OLV can result in down-regulated CCSP expressions andup-regulated C-PLA2 expressions in rabbit lung
tissues. Sevoflurane can protect against OLV-induced acute lung injury possibly by inhibiting C-PLA2 expression via
up-regulation of CCSP expressions or through other mechanisms resulting in down-regulated expression of C-PLA2.