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机构地区:[1]第一军医大学南方医院整形外科,广州510515
出 处:《中华整形外科杂志》2001年第3期154-156,共3页Chinese Journal of Plastic Surgery
基 金:国家自然科学基金!资助 (39870 80 7)
摘 要:目的 判断瘢痕疙瘩成纤维细胞Fas介导的死亡信号通道是否有阻断及阻断的具体位点 ,检测和比较FasMcab作用后增生性瘢痕和瘢痕疙瘩成纤维细胞内神经酰胺的变化。方法 取手术切除的增生性瘢痕和瘢痕疙瘩组织各 6例 ,通过细胞培养 4~ 6代后 ,不同浓度梯度的FasMcab处理增生性瘢痕及瘢痕疙瘩成纤维细胞。在一定的反应体系内 ,抽提细胞内神经酰胺 ,与外源性32 P ATP反应 ,通过放射自显影、闪烁记数等半定量、定量地反应胞内神经酰胺的含量。结果 增生性瘢痕成纤维细胞随着FasMcab浓度梯度的增高 ,其胞内神经酰胺的含量不断增高 ;瘢痕疙瘩成纤维细胞在各种浓度梯度下 ,胞内神经酰胺的含量无增加 ,各组间差异无显著性意义。结论 作为Fas介导的死亡信号通道中的第二信使 ,神经酰胺在瘢痕疙瘩成纤维细胞内的产生有缺陷。因此 ,Fas介导的瘢痕疙瘩成纤维细胞死亡信号传导阻滞是“上游”事件。Objective Our previous studies have shown that the FasMcab can not induce normal apoptosis of fibroblasts derived from keloids.To explore the concrete occlusive location,we investigated the responses of intracellular ceramide to different concentrations of FasMcab in fibroblasts derived from hypertrophic scar and keloid. Methods Samples of hypertrophic scars and keloids,six of each,were collected.Through cell culture for 4|6 generations,fibroblasts were selected for experiment The fibroblasts derived from these samples were exposed to different concentrations of FasMcab for 20 minutes and then intracellular ceramide was quantified by diacylglycerol kinase assay. Results Exposed to different concentrations of FasMcab,the intracellular ceramide increased prominently in hypertrophic scar|derived fibroblasts but no changes were seen in keloid|derived fibroblasts. Conclusion As the second messenger of the “Death” signal transduction mediated by Fas,the production of ceramide may be deficient in keloid|derived fibroblasts exposed to FasMcab.The occlusion of the “Death” signal transduction mediated by Fas may take place upriver.;
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