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目的探讨注射用红花黄色素对油酸致大鼠急性肺损伤的作用及其机制。方法Wistar大鼠随机分成对照组、油酸组(模型组)、油酸+山莨菪碱10mg/kg组、油酸+红花黄色素(8、16、32mg/kg)组,每组12只,各组在iv油酸0.18g/kg前给予药物干预。油酸损伤4h后,测定大鼠动脉血血氧分压、左肺含水系数和肺组织髓过氧化物酶(MPO)活性;RT-PCR法检测肺组织肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)mRNA表达水平;免疫组织化学法观察肺组织NF-κBp65活化细胞数;Western blotting法检测p38MAPK蛋白磷酸化水平。结果红花黄色素组大鼠动脉血血氧分压值均高于模型组,肺组织含水系数和MPO活性均低于模型组;同时各炎症因子mRNA表达水平,NF-κBp65阳性细胞数和p38MAPK蛋白磷酸化水平也均低于模型组。结论红花黄色素可缓解急性肺损伤所致肺水肿,提高动脉血氧分压,减少肺部炎性细胞浸润,其作用机制可能与抑制p38MAPK磷酸化及NF-κB活化,下调TNF-α、IL-β等炎症因子的表达有关。
Objective To investigate the effect and mechanism of safflor yellow injection on acute lung injury induced by oleic acid in rats. Methods Wistar rats were randomly divided into control group, oleic acid group (model group), oleic acid + anisodamine 10mg / kg group, oleic acid + safflower yellow pigment (8,16,32mg / kg) , And each group was given drug intervention before iv oleic acid 0.18g / kg. After 4 hours of oleic acid injury, the arterial partial pressure of blood oxygen, the left lung water content and the activity of myeloperoxidase (MPO) in the lung tissue were determined. The levels of tumor necrosis factor-α (TNF-α) , Interleukin-1β (IL-1β), interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM- The number of NF-κBp65-activated cells in lung tissue was detected by immunohistochemistry. The phosphorylation of p38MAPK protein was detected by Western blotting. Results The arterial partial pressure of blood oxygen of the safflower yellow group was higher than that of the model group, the water content and the MPO activity of the lung tissue were lower than the model group. At the same time, the expression of inflammatory cytokines mRNA, the number of NF-κBp65 positive cells and p38MAPK Protein phosphorylation levels were also lower than the model group. Conclusions Safflower yellow can relieve pulmonary edema induced by acute lung injury, increase arterial partial pressure of oxygen and decrease inflammatory cell infiltration in lung. Its mechanism may be related to inhibition of phosphorylation of p38MAPK and activation of NF-κB, down-regulation of TNF-α, IL-β and other inflammatory factors related to the expression.