论文部分内容阅读
目的:观察红霉素能否改善急性百草枯中毒性肺损伤。方法:①建立红霉素干预百草枯所致肺损伤的模型,将18只建康SD大鼠随机分成3组:A组为生理盐水组;B组为百草枯中毒组;C组为红霉素预先处理加百草枯中毒组。于相应时间点处死动物,取其肺组织。观察各组大鼠肺组织细胞间粘附分子-1(ICAM-1)表达、髓过氧化物酶(MPO)活性水平,光镜下肺组织病理改变及肺损伤评分。②从细胞分子水平观察红霉素干预百草枯所致肺损伤的机制:采用植块法培养大鼠肺微血管内皮细胞(PMVEC),观察红霉素对PMVEC表面ICAM-1表达的影响。结果:①B组、C组ICAM-1表达及MPO活性水平较A组升高,但C组又低于B组,组间比较均有显著性差异(P<0.05)。C组肺损伤的程度较B组有明显改善。②一定浓度范围的百草枯对PMVEC具有毒性作用,呈时间和浓度依赖性。红霉素(5μg/mL)可减弱百草枯(5.0×10-5mmol/L)诱导PMVEC表达ICAM-1。结论:红霉素可能通过抑制肺微血管内皮细胞ICAM-1的表达,削弱白细胞与内皮细胞之间的过度粘附,而对百草枯所致肺损伤具有一定保护作用。
Objective: To observe whether erythromycin can improve acute paraquat poisoning lung injury. Methods: ① To establish a model of erythromycin-induced lung injury induced by paraquat, 18 Jiankang SD rats were randomly divided into three groups: A group was saline group; B group was paraquat poisoning group; C group was erythromycin group Pretreatment plus paraquat poisoning group. Animals were sacrificed at the appropriate time points and their lung tissues were taken. The expression of intercellular adhesion molecule-1 (ICAM-1), the activity of myeloperoxidase (MPO), the pathological changes of lung tissue under light microscope and the lung injury score were observed. (2) To observe the mechanism of erythromycin intervention on paraquat-induced lung injury at the cellular and molecular level: Rat pulmonary microvascular endothelial cells (PMVEC) were cultured by explant method to observe the effect of erythromycin on ICAM-1 expression on PMVEC surface. Results: ① The expression of ICAM-1 and the activity of MPO in group B and C were higher than those in group A, but lower in group C than in group B (P <0.05). The degree of lung injury in group C was significantly improved compared with that in group B. Paraquat at a certain concentration range had toxic effects on PMVEC in a time and concentration-dependent manner. Erythromycin (5μg / mL) attenuated paraquat (5.0 × 10-5mmol / L) induced PMVEC expression of ICAM-1. CONCLUSION: Erythromycin may protect against paraquat-induced lung injury by inhibiting the expression of ICAM-1 in pulmonary microvascular endothelial cells, weakening the excessive adhesion between leukocytes and endothelial cells.