Liu Rui, Luo Jing, Li Jiang, Ma Qingjie, Sun Jingzhe, Li Yanhua, Wang Dianhua
Kunming Medical University, Kunming, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2013 May;33(5):625-30.
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.
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.
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).
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.
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。
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。
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)。
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。