PDTC对大鼠放射性肺损伤的保护作用及其机制

发布时间：2018-05-14 23:35

本文选题：放射性肺损伤 + 氢吡咯二硫代氨基甲酸酯　；参考：《山东医药》2017年32期

【摘要】：目的探讨氢吡咯二硫代氨基甲酸酯(PDTC)对大鼠放射性肺损伤的保护作用及其对肺组织核因子κB(NF-κB)、细胞间黏附分子1(ICAM-1)表达的影响。方法将60只Wistar大鼠随机分为正常对照组、模型组和PDTC组,每组20只。模型组、PDTC组采用6 MV X射线照射双肺制作放射性肺损伤模型。PDTC组照射前3天开始皮下注射PDTC 10 mg/kg,持续至照射后30天。正常对照组和模型组同期注射等体积生理盐水。各组照射开始后8、24周处死后取肺组织,部分右肺组织行HE、Masson染色,观察肺组织病理变化;取右肺中上叶,检测羟脯氨酸表达;取左肺组织,称湿重,计算肺系数;取右肺下叶,检测肺组织ICAM-1、NF-κB mRNA表达。结果正常对照组右肺组织均未见明显异常。照射开始后8周,模型组肺组织病变以渗出为主,并出现少许胶原纤维沉积;照射开始后24周,肺泡壁增厚,肺泡腔明显变小,肺间质内各种细胞成分增多,可见明显的局部灶性纤维化区域。PDTC组照射开始后8、24周肺组织病变较模型组同期明显减轻,纤维化增厚主要集中在支气管及血管外膜,肺泡区域几乎未见明显纤维化。模型组照射开始后8、24周肺组织羟脯氨酸表达、肺系数均高于正常对照组(P均0.05),PDTC组各时间点肺组织羟脯氨酸表达、肺系数较模型组同时间点明显降低(P均0.05),但仍高于正常对照组同时间点(P均0.05)。模型组照射开始后8、24周肺组织ICAM-1、NF-κB mRNA相对表达量均高于正常对照组同时间点(P均0.05),PDTC组各时间点肺组织ICAM-1、NF-κB mRNA相对表达量均较模型组同时间点降低(P均0.05),且高于正常对照组(P均0.05)。结论 PDTC能减轻放射性肺损伤大鼠的肺部炎症和纤维化程度,其机制可能与抑制NF-κB活化、调控ICAM-1表达有关。
[Abstract]:Objective to investigate the protective effect of hydropyrrolidine dithiocarbamate (PDTC) on radiation induced lung injury in rats and its effect on the expression of nuclear factor 魏 B (NF- 魏 B) NF- 魏 B, an intercellular adhesion molecule (ICAM-1). Methods 60 Wistar rats were randomly divided into normal control group, model group and PDTC group with 20 rats in each group. Radiation-induced lung injury model was induced by 6 MV X-ray irradiation in PDTC group. PDTC 10 mg / kg was injected subcutaneously 3 days before irradiation in PDTC group until 30 days after irradiation. The normal control group and the model group were injected with the same volume of saline at the same time. Eight weeks after irradiation, lung tissue was taken out, and some of the right lung tissues were stained with HE Masson to observe the pathological changes of the lung tissue; the middle and upper lobe of the right lung was taken to detect the expression of hydroxyproline; the left lung tissue was taken to weigh wet and calculate the lung coefficient; the lower lobe of the right lung was taken from the lower lobe of the right lung. The expression of NF- 魏 B mRNA in lung tissue was detected. Results there was no obvious abnormality in the right lung tissue in the normal control group. At 8 weeks after irradiation, the pathological changes of lung tissue in the model group were mainly exudate, and a little collagen fiber was deposited. 24 weeks after irradiation, the alveolar wall was thickened, the alveolar cavity was obviously smaller, and the various cellular components in the interstitial lung were increased. The pathological changes of lung tissue in PDTC group at 824 weeks after irradiation were obviously reduced compared with that in model group. The thickening of fibrosis was mainly concentrated in the bronchi and adventitia, and there was almost no obvious fibrosis in alveolar region. The lung hydroxyproline expression in the model group was significantly higher than that in the normal control group at 24 weeks after irradiation. Compared with the model group, the lung coefficient was significantly lower than that of the model group at the same time point (P < 0.05), but still higher than that of the normal control group at the same time point (P < 0.05). The relative expression of ICAM-1 NF- 魏 B mRNA in lung tissue in the model group was significantly higher than that in the normal control group at 24 weeks after irradiation (P < 0.05). The relative expression of ICAM-1NF- 魏 B mRNA in the lung tissue in the model group was lower than that in the model group at the same time point (P 0.05) and higher than that in the normal control group (P < 0.05). Conclusion PDTC can attenuate the degree of pulmonary inflammation and fibrosis in rats with radiation-induced lung injury. The mechanism may be related to the inhibition of NF- 魏 B activation and the regulation of ICAM-1 expression.
【作者单位】：沈阳市第七人民医院;郑州大学第五附属医院;
【分类号】：R730.55

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