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Wistar大鼠的咬肌放射损伤模型

A Wistar rat model of radiation-induced masseter injury
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摘要 背景:构建稳定可靠的咬肌放射损伤模型对颌面部肿瘤放疗的相关研究有重要意义。目的:以放射剂量40Gy照射后Wistar大鼠咬肌构建大鼠咬肌放射损伤模型。方法:成年Wistar大鼠20只,随机分成正常对照组和放射损伤组。放射损伤组采用直线加速器照射大鼠咬肌区累积40Gy制造咬肌放射损伤。在28d后,在光镜及电镜下观察咬肌放射区病理改变,RT-PCR检测转化生长因子β1的基因表达。结果与结论:40Gy照射后28d大鼠咬肌区出现结构受损、血管密度减低(P<0.01)等放射损伤表现,同时引起转化生长因子β1的基因表达升高(P<0.001)等机体被动修复表现。结果证实Wistar大鼠咬肌区直线加速器40Gy照射可以作为咬肌放射损伤模型。 BACKGROUND: Construction of a stable animal model of radiation-induced masseter injury is significant for the research of maxillofacial region tumor. OBJECTIVE: To establish the animal model of Wistar rats with radiation-induced masseter injury after irradiated with the radiation dose of 40 Gy. METHODS: A total of 20 male adult Wistar rats were selected and randomly divided into radiation injury group and control group. Radiation injury group was radiated with linear accelerator at a dose of 40 Gy in the masseter tissue. After irradiated for 28 days, pathological changes in the masseter tissue of the radiation injury group and control group were observed by light microscope and electron microscope; the gene expression of transforming growth factor-β1 was detected by reverse transcription-PCR. RESULTS AND CONCLUSION: After irradiated for 28 days at the dose of 40 Gy, the irradiation injury of structural damage and reduced vascular density were observed in the masseter tissue (P 〈 0.01), and the gene expression of transforming growth factor-β1 was increased (P 〈 0.001 ). The result indicates thatmasseter tissue irradiated with linear accelerator at a dose of 40 Gy can be considered as the model of radiation-induced masseter injury.
出处 《中国组织工程研究》 CAS CSCD 2013年第24期4515-4520,共6页 Chinese Journal of Tissue Engineering Research
基金 青岛市科技局项目(08-2-1-5-nsh 11-2-3-2-(7)-nsh) 青岛市卫生局项目(2008-wsj024 2012-wsj051)~~
关键词 组织构建 组织构建实验造模 放射损伤 动物模型 转化生长因子Β1 血管密度 咬肌 放射疗法 颌面部 超微结构 基因表达 病理改变 其他基金 tissue construction experimental modeling in tissue construction radiation injury animal model transforming growth factor-beta 1 vascular density masseter radiation therapy maxillofacial ultrastructure gene expression pathological changes other grants-supported paper
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