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作 者:徐少骏[1] 滕建英[2] 谢菁[1] 吴艾竞[1] 陈东明[3] 鲍卫汉[3]
机构地区:[1]杭州市第二人民医院整形外科,杭州310015 [2]杭州师范学院临床医学院 [3]北京大学第三临床医学院
出 处:《中华整形外科杂志》2008年第1期46-49,共4页Chinese Journal of Plastic Surgery
摘 要:目的探讨对瘢痕疙瘩和增生性瘢痕成纤维细胞在激素和干扰素α-2b(IFNα-2b)作用后是否产生凋亡,以及相关细胞信号传导通路的激活或抑制是否一致。方法对6例瘢痕疙瘩、增生性瘢痕及6例皮肤标本,采用细胞培养、免疫组织化学、凝胶电泳及FACE ELISA方法通过检测Bax和Bcl-2蛋白表达、特异性DNA梯状条带以及激活(磷酸化)的ERK1/2和JNK的吸光度A值,对不同成纤维细胞在地塞米松(0.1mg/ml)和干扰素α-2b(1000U/ml)作用后的细胞凋亡及相关细胞信号传导通路进行了研究。结果地塞米松可通过激活ERK1/2和JNK细胞传导通路诱导三类不同来源成纤维细胞发生细胞凋亡;干扰素α-2b不能诱导这三类不同来源成纤维细胞发生明显细胞凋亡,且IFN α-2b抑制增殖瘢痕的ERK1/2通路,而对JNK通路无影响,其不引起正常皮肤成纤维细胞ERK1/2和JNK通路的变化。结论激素类药物和干扰素α-2b对瘢痕疙瘩、增生性瘢痕和正常皮肤成纤维细胞的作用机制不同。Objective This paper is to investigate the effects of steroid or IFN α-2b on apoptosis and cell pathway of fibroblasts from keloids, hypertrophic scars and normal skins and different responses of different fibroblasts. Methods 6 samples from keloid, hypertrophic scar and normal skin were collected respectively and fibroblasts from different sources were cultured in vitro. After different fibroblasts were treated with dexamethasone (0.1 mg/ml) or IFN α-2b ( 1 000 U/ml), Bax and Bcl-2 protein expressions were detected in situ by immunohistochemical staining; DNA ladders of different fibroblasts were observed by gel electrophoresis; and relative activated (phospho-) ERK1/2 and JNK pathways were detected by method of FACE EUSA. Results Dexamethasone could induce apoptosis of fibroblasts from keloids, hypertrophic scars and normal skins through activating (phospho-) ERK1/2 and JNK pathways; IFN α-2b could not induce apoptosis of fibroblasts from different sources. IFN α-2b could inhibit (phospho-) ERK1/2 pathway and could not affect (phospho-) JNK pathways of fibroblasts from keloid and hypertrophic scar. IFN α-2b could affect neither (phospho-) ERK1/2 pathway nor (phospho-) JNK pathways of fibroblasts from normal skin. Conclusions The responses of different fibroblasts to steroid or IFN α-2b were different.
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