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An Experimental Study of Pathogenesis of Steroid-induced Avascular Necrosis of Femoral Head

机译:类固醇激素引起的股骨头坏死的发病机制的实验研究

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Objective: To explore the pathogenesis of avascular necrosis of femoral head (ANFH) and search an effective method for clinical practice. Methods: Twenty-four Japanese rabbits were divided into 2 groups of models and controls. ANFH models were produced by intramuscular-injection of large dosage of steroid to rabbits for 8 weeks. From the 4th, 8th and 12th week after production of models, 2 rabbits of each group were sacrificed to observe the structure of femoral head through light microscope and scanning electron microscope. The contents of Nitric Oxide (NO), tissue-type plasminogen activator (t-PA) and -plasminogen activator inhibitor (PAI) in plasma of the 4 rabbits in each group were estimated at the same time. Results: Compared with control group, the rabbits of model group exhibited many differences: such as osteoporosis of femoral head, the presence of more bone lacuna and fat cell through light microscope observing; the broken and sunk bone trabecula, the loosen and broken collagen fibers on the surface of bone matrix through scanning electron microscope observing. Compared with control group, the Concentration of NO and t-PA in plasma of the model rabbits decreased obviously, but the Concentration of the PAI increased obviously. Conclusion: The steroid-induced ANFH might be related to the lower level of NO and the descent of fibrinolytic activity.
机译:目的:探讨股骨头缺血性坏死(ANFH)的发病机制,寻找有效的临床实践方法。方法:将24只日本兔分为模型和对照组两组。 ANFH模型是通过向兔子肌肉内注射大剂量的类固醇8周而产生的。从制作模型的第4、8和12周起,处死每组2只兔子,通过光学显微镜和扫描电子显微镜观察股骨头的结构。同时估算每组四只家兔血浆中一氧化氮(NO),组织型纤溶酶原激活物(t-PA)和-纤溶酶原激活物抑制剂(PAI)的含量。结果:与对照组相比,模型组兔表现出许多差异:通过光镜观察可见股骨头骨质疏松,存在更多的骨腔和脂肪细胞。通过扫描电子显微镜观察,骨小梁的断裂和下沉,骨基质表面胶原纤维的松弛和断裂。与对照组相比,模型兔血浆中NO和t-PA的浓度明显降低,而PAI的浓度则明显升高。结论:类固醇诱导的ANFH可能与NO水平降低和纤溶活性下降有关。

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