中国组织工程研究与临床康复
中國組織工程研究與臨床康複
중국조직공정연구여림상강복
JOURNAL OF CLINICAL REHABILITATIVE TISSUE ENGINEERING RESEARCH
2011年
15期
2842-2846
,共5页
沈宗泽%郑建金%贾暮云%董刚%李涛
瀋宗澤%鄭建金%賈暮雲%董剛%李濤
침종택%정건금%가모운%동강%리도
放射损伤%大鼠%毛细血管损伤%转化生长因子β1%血管密度
放射損傷%大鼠%毛細血管損傷%轉化生長因子β1%血管密度
방사손상%대서%모세혈관손상%전화생장인자β1%혈관밀도
背景:长期的放射线累积更可引起周围组织纤维化,张口受限,严重影响肿瘤患者的生活品质.目的:观察大鼠咀嚼肌放射损伤后软组织的病理改变及体内转化生长因子β1 mRNA的表达.方法:成年Wistar大鼠30只,随机分成对照组(n=10)和放射组(n=20).放射组利用直线加速器累积照射咀嚼肌40 Gy.光镜和电镜下观察咀嚼肌放射损伤区血管病理改变及RT-PCR检测咀嚼肌放射损伤区转化生长因子β1基因表达.结果与结论:放射组咀嚼肌放射损伤区毛细血管密度较对照组明显降低(P < 0.01),转化生长因子β1 mRNA水平较对照组显著升高(P < 0.01).提示放射损伤可促使组织纤维化修复放射损伤.
揹景:長期的放射線纍積更可引起週圍組織纖維化,張口受限,嚴重影響腫瘤患者的生活品質.目的:觀察大鼠咀嚼肌放射損傷後軟組織的病理改變及體內轉化生長因子β1 mRNA的錶達.方法:成年Wistar大鼠30隻,隨機分成對照組(n=10)和放射組(n=20).放射組利用直線加速器纍積照射咀嚼肌40 Gy.光鏡和電鏡下觀察咀嚼肌放射損傷區血管病理改變及RT-PCR檢測咀嚼肌放射損傷區轉化生長因子β1基因錶達.結果與結論:放射組咀嚼肌放射損傷區毛細血管密度較對照組明顯降低(P < 0.01),轉化生長因子β1 mRNA水平較對照組顯著升高(P < 0.01).提示放射損傷可促使組織纖維化脩複放射損傷.
배경:장기적방사선루적경가인기주위조직섬유화,장구수한,엄중영향종류환자적생활품질.목적:관찰대서저작기방사손상후연조직적병리개변급체내전화생장인자β1 mRNA적표체.방법:성년Wistar대서30지,수궤분성대조조(n=10)화방사조(n=20).방사조이용직선가속기루적조사저작기40 Gy.광경화전경하관찰저작기방사손상구혈관병리개변급RT-PCR검측저작기방사손상구전화생장인자β1기인표체.결과여결론:방사조저작기방사손상구모세혈관밀도교대조조명현강저(P < 0.01),전화생장인자β1 mRNA수평교대조조현저승고(P < 0.01).제시방사손상가촉사조직섬유화수복방사손상.
BACKGROUND: Long-term radioactive ray accumulation leads to surrounding tissues fibrosis accompanied by limitation of mouth-opening, which seriously affects life quality of tumor patients. OBJECTIVE: To observe pathological change of soft tissues in rats with radiation masseter injury and the level of transforming growth factor β1 (TGF-β1) mRNA expression in vivo.METHODS: A total of 30 Wistar rats were randomly divided into control group (n=10) and radiated group (n=20). Radiated group were radiated with linear accelerator at a dose of 40 Gy. The pathological changes of vessels were observed under light microscope and electron microscope and expression of TGF-β1 was detected by RT-PCR. RESULTS AND CONCLUSION: The microvessel density of radiated group was obviously decreased than that of the control group (P < 0.01), but the mRNA expression of was higher than that in the control group (P < 0.01). It suggests that radiated injury can induce fibrosis to repair the radiated injury.