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七氟醚对单肺通气所致急性肺损伤的保护机制:环氧合酶-2和5-脂氧合酶途径的作用

Protective mechanisms of sevoflurane against one-lung ventilation-induced acute lung injury: role of cyclooxygenase-2 and 5-lipoxygenase pathways.

作者信息

Liu Rui, Luo Jing, Li Jiang, Ma Qingjie, Sun Jingzhe, Li Yanhua, Wang Dianhua

机构信息

Kunming Medical University, Kunming, China.

出版信息

Nan Fang Yi Ke Da Xue Xue Bao. 2013 May;33(5):625-30.

PMID:23688977
Abstract

OBJECTIVE

To explore the protective mechanisms of sevoflurane against acute lung injury (ALI) induced by one-lung ventilation (OLV) in view of cyclooxygenase-2 (COX2) and 5-lipoxygenase (5-LOX) pathways.

METHOD

Eighteen healthy Japanese white rabbits were randomized into sham-operated group (S group), OLV group (O group) and OLV + sevoflurane group (OS group). COX2 and 5-LOX protein and mRNA expressions in the lungs were detected by Western blotting and real-time PCR, respectively. Prostaglandin I2 (PGI2), thromboxane A2 (TXA2) and leukotrienes B2 (LTB2) in the lung tissues were quantified with ELISA. Histological scores and lung wet/dry weight (W/D) ratios were determined for lung injury assessment.

RESULTS

COX2 and 5-LOX protein and mRNA expressions and the contents of LTB2, TXA2 and PGI2 in the lungs, lung W/D ratio and histological scores were significantly higher while PGI2/TXA2 ratio was significantly lower in O group and OS group than in S group (P<0.05). Compared with those in O group, COX2 and 5-LOX expressions, pulmonary contents of LTB2, TXA2 and PGI2, and lung W/D ratio all decreased significantly but PGI2/TXA2 ratio was significantly elevated in OS group (P<0.05).

CONCLUSION

OLV may activate COX2 and 5-LOX pathways to result in increased production of arachidonic acid metabolites. Sevoflurane protects against OLV-induced ALI probably by reducing AA metabolites and regulating PGI2/TXA2 ratio through inhibitions of COX2 and 5-LOX pathways.

摘要

目的

从环氧化酶 -2(COX2)和5 -脂氧合酶(5 - LOX)途径探讨七氟醚对单肺通气(OLV)所致急性肺损伤(ALI)的保护机制。

方法

将18只健康日本白兔随机分为假手术组(S组)、OLV组(O组)和OLV +七氟醚组(OS组)。分别采用蛋白质免疫印迹法和实时荧光定量PCR检测肺组织中COX2和5 - LOX蛋白及mRNA表达。采用酶联免疫吸附测定法对肺组织中的前列腺素I2(PGI2)、血栓素A2(TXA2)和白三烯B2(LTB2)进行定量分析。测定组织学评分和肺湿/干重(W/D)比值以评估肺损伤情况。

结果

O组和OS组肺组织中COX2和5 - LOX蛋白及mRNA表达、LTB2、TXA2和PGI2含量、肺W/D比值及组织学评分均显著高于S组(P<0.05),而PGI2/TXA2比值显著低于S组(P<0.05)。与O组相比,OS组COX2和5 - LOX表达、肺组织中LTB2、TXA2和PGI2含量及肺W/D比值均显著降低(P<0.05),但PGI2/TXA2比值显著升高(P<0.05)。

结论

OLV可能激活COX2和5 - LOX途径,导致花生四烯酸代谢产物生成增加。七氟醚可能通过抑制COX2和5 - LOX途径减少花生四烯酸代谢产物并调节PGI2/TXA2比值,从而对OLV诱导的ALI起到保护作用。

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