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作 者:秦全红[1] 王德文[1] 高亚兵[1] 彭瑞云[1] 谷庆阳[1] 夏国伟[1] 崔雪梅[1]
机构地区:[1]军事医学科学院放射医学研究所,北京100850
出 处:《辐射研究与辐射工艺学报》2003年第2期125-130,共6页Journal of Radiation Research and Radiation Processing
基 金:全军九五重点招标课题基金 (96Z008) 资助
摘 要:探讨了局部照射对伤口愈合过程中成纤维细胞(Fibroblast, Fb)长消规律、形态学及超微结构的影响。将156只Wistar大鼠随机分为单纯创伤组(对照组)和照射复合创伤组(照射组),采用光镜、电镜和免疫组化方法研究两组伤口愈合中成纤维细胞病理变化、超微结构及α-actin表达。结果表明,对照组伤口成纤维细胞数量于伤后1—10d呈进行性增加,伤后10d达高峰,照射组成纤维细胞数量于伤后1—15d较对照组减少且高峰后移,伤后15d达高峰。依据超微结构特点成纤维细胞分为过渡型、增殖型、合成分泌旺盛型、肌成纤维细胞型、转归型和凋亡型六种类型。在伤愈不同时期各种类型分布不同,照射组各型成纤维细胞出现滞后,尤其是合成分泌旺盛型和肌成纤维细胞型,并出现畸形成纤维细胞。后者细胞大小形态各异,内质网高度扩张,高尔基体和微丝束减少等。照射抑制伤口成纤维细胞增殖,使各型成纤维细胞出现滞后,并使成纤维细胞形态发生变化,出现特有的畸形成纤维细胞。The paper is to study the number, morphology and ultrastructure of fibroblasts in the process of wound healing of local irradiated rats. 156 Wistar rats were divided into two groups, the wound group (control) and the radiation-combined wound group (radiation group). Numeral, morphological and ultrastructural changes of the fibroblasts were observed with light microscope and transmission electron microscope. The α-SM actin expression in the fibroblasts was measured with immunohistochemecal assay. The number of the fibroblasts in the control group increased gradually and reached to the max on the 10th day. In the radiation group, the fibroblasts number changed less than the control and the peak was seen on the 15th day. The fibroblasts included types of the transition, the proliferation, the synthesis-secretion, the myofibroblast, the transformation and the apoptosis. For the radiation group, each of the six types of fibroblasts, especially the synthesis-secretion type and the myofibroblast type, appeared later in comparison with the control. In addition, the peculiarities of the abnormal fibroblasts could be observed in the radiation group, the highly expanded rough endoplastmic reticulums, the less golgis and microfilaments. Irradiation can inhibit the proliferation of the fibroblasts, delay the appearance of the stage-specific fibroblasts, cause the morphological and ultrastructural changes in the fibroblasts and promote the formation of the abnormal fibroblasts.
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