前列腺素E_1对大鼠移植肺再灌注损伤的保护作用

Protective effects of prostaglandin E_1 on ischemia/reperfusion-induced lung injury after lung transplantation in rats

目的:探讨前列腺素E1(PGE1)对大鼠移植肺再灌注损伤的保护作用及机制。方法:SD大鼠36只随机分为3组,每组12只,即对照组、肺移植组和肺移植加PGE1处理组,观察受体大鼠肺移植前后注射PGE1对移植肺再灌注损伤的保护作用。肺功能指标包括肺湿干重比、肺通透性指数、支气管肺泡灌洗液(BALF)中白细胞计数和分类。比色法检测各组肺组织超氧化物歧化酶(SOD)和丙二醛(MDA)含量。ELISA法检测受体大鼠血清中肿瘤坏死因子α(TNFα)含量。结果:肺移植术后1 h,肺湿干重比、肺通透指数、BALF中中性粒细胞百分比和MDA含量显著高于对照组(P<0.01),肺组织中SOD活性明显低于对照组(P<0.01);给予受体大鼠静脉注射PGE1可明显改善上述指标(P<0.01);肺移植组血清TNFα含量较对照组显著升高(P<0.01),PGE1可明显降低血清TNFα水平(P<0.01)。结论:PGE1对移植肺缺血／再灌注损伤有显著的保护作用,与其抗氧化自由基损伤、抑制中性白细胞激活和炎性因子TNFα分泌有关。

AIM: To investigate the protective effects and the mechanisms of prostaglandin E1 (PGE1 ) on ischemia/reperfusion (I/R)-induced lung injury after lung transplantation in rats. METHODS: 36 SD rats were randomly divided into 3 groups ( n = 12 in each) : sham operation group ( control group) , lung transplantation (LT)group and PGE1 treatment group. PGE1 was administered to the rats through intra-venous way from 10 min before the operation to the end of the reperfusion. The wet/dry ratio of lung, lung permeability index and neutro-phil percentage were detected in bronchoalveolar lavage fluid (BALE). Superoxide dismutase (SOD) and malond-ialdehyde (MDA) of lung tissue were measured by color-imetry. Serum level of tumor necrosis factor α(TNFα)was detected by enzyme-linked immunosorbent assay (ELISA). RESULTS: The wet/dry ratio of lung, lungpermeability index and neutrophils percentage in BALF and MDA content of lung tissue in LT group were higher than those in control group( P < 0.01) . SOD activity of lung tissue in LT group was lower than that in control group( P < 0.01) . Administration of PGE1 improved the indexes above ( P < 0.01). Serum level of TNFα increased after lung transplantation compared with the control group. However, PGE1 treatment reduced the serum level of TNFα(P<0.01). CONCLUSION: PGE1 can protect the lung function against I/R injury after lung transplantation. The mechanism is related to its anti-oxi-dative effect and the inhibition of TNFα release and neutrophils activation.