PET-CT观察矽肺动物模型可行性研究
本文选题:矽肺 + 动物模型 ; 参考:《中国职业医学》2017年03期
【摘要】:目的探讨采用小动物正电子发射计算机断层显像(PET)-计算机体层扫描(CT)动态观察活体大鼠矽肺模型的可行性。方法无特定病原体级SD大鼠分为模型组和对照组,模型组一次性气管内注入质量浓度为30 g/L的矽尘混悬液建立大鼠矽肺模型,对照组予等体积的0.9%氯化钠溶液。2组大鼠均于造模后第1、2、3、4、6、8和12周分别随机选取6只,以小动物PET-CT进行肺部CT检查并检测CT值,同时进行PET检查并检测氟-18-氟代脱氧葡萄糖标准化摄取值(SUV)。扫描后处死大鼠,检测肺脏脏器系数,进行肺脏病理组织学观察,检测血清转化生长因子β1(TGF-β1)、白细胞介素1(IL-1)和肺组织羟脯氨酸(HYP)水平。结果模型组大鼠肺脏病理组织学改变在早期表现为肺组织炎症性渗出,随着时间延长,炎症反应逐渐减轻,而肺间质纤维化逐渐明显;PET-CT影像学表现与病理组织学改变基本一致。模型组大鼠肺部SUV在第1~3周3个时间点均高于同时间点对照组(P0.05),且在第1~4周随染尘时间的增加而下降(P0.05)。模型组大鼠肺部CT值在7个时间点均高于同时间点对照组(P0.05),且在第1~6周随染尘时间的增加而下降(P0.05),在第6~12周随染尘时间的增加而升高(P0.05)。模型组大鼠肺脏脏器系数和肺组织HYP水平在7个时间点均高于同时间点对照组(P0.05),且在第1~4周肺脏脏器系数随染尘时间的增加而下降(P0.05),在第6~12周肺组织HYP水平随染尘时间的增加而升高(P0.05)。除第3和4周外,模型组大鼠血清TGF-β1水平在其余5个时间点均高于同时间点对照组(P0.05),且在第1~4周随染尘时间的增加而下降(P0.05),在第4~8周随染尘时间的增加而升高(P0.05);模型组大鼠血清IL-1水平在第1~4周4个时间点均高于同时间点对照组(P0.05),且随染尘时间的增加而下降(P0.05)。结论小动物PET-CT可有效观察活体矽肺模型大鼠肺部早期炎症和晚期纤维化,可作为动态追踪矽肺大鼠模型肺部损伤的检测方法。
[Abstract]:Objective to investigate the feasibility of using positron emission computed tomography (PET) in small animals to dynamically observe the model of silicosis in vivo in rats. Methods Sprague-Dawley rats with no specific pathogens were divided into two groups: model group and control group. In the model group, the silicosis model was established by injecting 30 g / L silica dust suspension into the trachea of the model group. The control group was treated with 0.9% sodium chloride solution of equal volume. 6 rats were randomly selected at 8 and 12 weeks after modeling. Lung CT was performed with small animal PET-CT and CT values were measured. At the same time, PET was performed to detect the standardized uptake of fluorine-18-fluorodeoxyglucose (F-18-fluorodeoxyglucose). After scanning, the rats were killed, the lung organ coefficient was measured, the histopathology of lung was observed, the serum levels of transforming growth factor 尾 1 (TGF- 尾 1), interleukin 1 (IL 1) and hydroxyproline (HYP) in lung tissue were detected. Results the pulmonary histopathological changes in the model group showed inflammatory exudation of lung tissue at the early stage, and the inflammatory reaction gradually decreased with the prolongation of time, while the pulmonary interstitial fibrosis gradually showed obvious PET-CT imaging findings consistent with the histopathological changes. The pulmonary SUV in the model group was significantly higher than that in the control group at three time points at the 1st week, and decreased with the increase of the dust exposure time at the 1st and 4th week. The lung CT value in the model group was higher than that in the control group at 7 time points, and decreased with the increase of dust exposure time at the 1st week, and increased with the increase of dust exposure time at the 6th week. The lung organ coefficient and HYP level of lung tissue in the model group were higher than those in the control group at 7 time points, and the lung organ coefficient decreased with the increase of dust exposure time in the 1st week and the lung tissue HYP level in the 6th week and the 12th week in the model group, and the lung tissue HYP level in the model group was higher than that in the control group at the same time point (P 0.05), and the lung organ coefficient decreased with the increase of dust exposure time at the 1st week. With the increase of dust time, P0. 05% was increased. Except for weeks 3 and 4, The serum TGF- 尾 1 level in the model group was higher than that in the control group at the other five time points, and decreased with the increase of dust exposure time at the 1st week, and increased with the dust exposure time at the 48th week, while the serum IL-1 level in the model group was higher than that in the control group. The four time points of the first week were higher than that of the control group at the same time point (P 0.05), and decreased with the increase of the time of dust exposure. Conclusion small animal PET-CT can effectively observe early inflammation and late fibrosis in lung of rats with silicosis in vivo, and can be used as a method to detect lung injury in silicosis model.
【作者单位】: 广东省职业病防治院广东省职业病防治重点实验室;贵州医科大学;广东省妇幼保健院;
【基金】:国家科技支撑计划项目(2014BAI12B01) 国家自然科学基金(81302396) 国家临床重点专科建设项目(2011-09) 广东省科技计划项目(2017A020215159) 广东省医学科研基金(B2016056) 广东省职业病防治重点实验室(2012A061400007)
【分类号】:R135.2;R-332
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