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目的观察褪黑素对博来霉素致大鼠肺纤维化p38丝裂原活化蛋白激酶(p38MAPK)表达的影响,从而探讨其防治肺间质纤维化的机制。方法雌性SD大鼠45只随机分为3组,每组15只,分别为模型组,干预组及对照组。模型组和干预组均一次性气管内注入博来霉素(5mg/kg),对照组气管注入同体积生理盐水。干预组于造模前2d腹腔注射褪黑素[4mg/(kg.d)],而模型组和对照组给予同体积生理盐水。每组分别于7、14、28d各随机处死5只大鼠。采用HE染色和M asson染色了解肺泡炎和肺纤维化的情况,用免疫组织化学方法检测肺组织p38MAPK和FN蛋白的表达;RT-PCR方法检测肺组织p38MAPK的水平。结果成功建立肺纤维化模型。肺组织中p38MAPK(蛋白和mRNA)和FN(蛋白)在对照组表达较弱,模型组在7d表达增强,14d明显增强,28d较14d开始减弱,干预组各期上升幅度均低于模型组,但仍强于正常组(P<0.05)。结论褪黑素可能通过抑制p38MAPK的表达而减少FN的分泌和沉积,延缓肺间质损害的进程。
Objective To investigate the effect of melatonin on the expression of p38 mitogen activated protein kinase (p38MAPK) induced by bleomycin-induced pulmonary fibrosis in rats, and to explore its mechanism of prevention and treatment of pulmonary fibrosis. Methods 45 female SD rats were randomly divided into 3 groups (n = 15 each), model group, intervention group and control group. Bleomycin (5mg / kg) was injected intratracheally into the model group and the intervention group, and the control group was injected with the same volume of normal saline. The intervention group was intraperitoneally injected with melatonin [4mg / (kg · d)] 2 days before modeling, while the model group and the control group were given the same volume of normal saline. Five rats were randomly sacrificed at 7, 14 and 28 days in each group. The expression of p38MAPK and FN protein in lung tissue was detected by immunohistochemistry and the level of p38MAPK in lung tissue was detected by RT-PCR. HE staining and M asson staining were used to detect the alveolitis and pulmonary fibrosis. Results Pulmonary fibrosis model was successfully established. The expression of p38MAPK (protein and mRNA) and FN (protein) in the lung tissue was weak in the control group. The expression of p38MAPK (protein and mRNA) in the lung tissue of the model group increased on the 7th day, increased significantly on the 14th day, decreased on the 28th day compared with the 14th day, But still stronger than the normal group (P <0.05). Conclusion Melatonin may reduce the secretion and deposition of FN by inhibiting the expression of p38MAPK, and delay the process of pulmonary interstitial damage.