摘要
目的:分析肿瘤坏死因子α受体1(TNF-αR1)在增生性瘢痕组织中基因表达情况,为今后从基因方面治疗增生性瘢痕提供依据。方法:选取48例增生性瘢痕组织患者为观察组(其中瘢痕组织增生时间1~3、4~6、7~12个月及1年以上各12例),12例正常瘢痕组织患者为对照组,以RT-PCR法对瘢痕组织中TNF-αR1 mRNA表达进行检测,比较各组TNF-αR1 mRNA水平差异。结果:对照组TNF-αR1 mRNA表达均高于观察组不同时间点TNF-αR1 mRNA表达,差异有统计学意义(P<0.05),且1年以上组织TNF-αR1 mRNA表达量均高于1~3、4~6、7~12个月组织(P<0.05)。结论:增生性瘢痕组织中TNF-αR1 mRNA表达低于正常瘢痕组织,同时随着时间增加增生性瘢痕中TNF-αR1 mRNA表达会显著上升。
Objective:To analyze the gene expression of tumor necrosis factor α receptor 1(TNF-αR1 in hypertrophic scar tissue,and to provide evidence for gene therapy of hypertrophic scar in the future.Method:48 patients with hypertrophic scar tissue were selected as observation group(the scar proliferation time at 1-3,4-6,7-12 months and over 1 year were occurred in 12 cases respectively)and 12 patients with normal scar tissue as control group.The expression of TNF-αR1 mRNA in scar tissue was detected by RT-PCR.The differences in TNF-αR1 m RNA levels among groups were compared.Result:The expression of TNF-αR1 mRNA in control group were higher than those of observation group at different time points(P<0.05),and the expression of TNF-αR1 mRNA in tissues over one year was higher than those of tissues over 1-3,4-6,7-12 months(P<0.05).Conclusion:The expression of TNF-αR1 mRNA in hypertrophic scar tissue was lower than that of normal scar tissue,at the same time,the expression of TNF-αR1 mRNA in hypertrophic scar increased significantly with time.
引文
[1]刘达恩,黎洪棉,梁自乾,等.TNF-αR1 mRNA和Caspase-10 mRNA在增殖期增生性瘢痕组织中的表达及意义[J].广西医学,2010,32(1):4-7.
[2]杨景山.医学细胞化学与细胞生物学技术[M].北京:北京医科大学中国协和医科大学联合出版社,1990:6-16.
[3]章建林,林子豪,江华,等.增生性瘢痕组织中肿瘤坏死因子αR1mRNA的表达及意义[J].中国临床康复,2004,8(17):3296-3297,3438.
[4]Peruccio D,Castagnolic C,Stella M,et al.Altered biosynthesis of tumor necrosis factor(TNF)alpha is involved in postburn hypertrophic scars[J].Burns,1994,20(2):118-121.
[5]章建林,林子豪,江华,等.增生性瘢痕组织中TNF-αm RNA的动态表达及临床意义[J].中华整形外科杂志,2004,20(1):56-58.
[6]章建林,林子豪,江华,等.增生性瘢痕组织中TNF-α基因的表达及其意义[J].第二军医大学学报,2005,26(1):48-50.
[7]Joyce D A,Steer J H,Abraham L J.Glucocorticoid modulation of human monocyte/macrophage function:control of TNF-alpha secretion[J].Inflamm Res,1997,46(11):447-451.
[8]高春芳,徐玲玲,王皓,等.正常皮肤与瘢痕组织成纤维细胞对细胞因子、细胞外间质和胶原基因启动子反应性比较研究[J].中华皮肤科杂志,2003,36(11):628-631.
[9]Duncan M R,Berman B.Differencial regulation of collagen,glycosaminoglycan,fibronection and collagenase activity production in cultured human adult dermal fibroblasts by interleukin1-αandβand TNF-αandβ[J].J Inest Dermatol,1989,92(5):699-706.
[10]杜逸凤,潘宁,吴冬梅.病理性瘢痕与多种细胞因子相关性的研究进展[J].实用医院临床杂志,2016,13(1):141-144.
[11]章建林,林子豪,江华,等.TNF-α及其受体TNF-αR1mRNA在增生性瘢痕组织中的表达及意义[J].中华物理医学与康复杂志,2004,26(5):266-268.
[12]袁瑞红,刘流,赵德萍,等.TNF-α对瘢痕成纤维细胞影响的研究[J].广东医学,2010,31(5):607-609.
[13]杨文玖,邹云雯,王志杰,等.肿瘤坏死因子-α对NIH3T3细胞成熟化作用的影响[J].齐鲁医学杂志,2010,25(3):235-237.
[14]石光清,支科.β射线敷贴照射治疗增生性瘢痕机制及与肿瘤坏死因子-α关系研究进展[J].中国现代医学杂志,2010,20(10):1546-1550.
[15]Zhang H G,Huang N,Liu D,et al.Gene therapy that inhibits nuclear translocation of nuclear fact or KB results in tumor necrosis factorα-induced apoptosis of human synovial fibroblasts[J].Arithritis Rheum,2000,43(5):1094-1105.
[16]陈钊,李小静,王晖.构建肿瘤坏死因子α刺激基因6慢病毒表达及干扰载体及对人瘢痕疙瘩成纤维细胞增殖与凋亡的影响[J].中国组织工程研究,2016,20(29):4319-4327.
[17]田小雨,李小静,李心怡,等.TSG-6调控PI3K/Akt-Bcl-2通路影响人瘢痕疙瘩凋亡机制的研究[J].安徽医科大学学报,2018,53(4):563-567.
[18]付晋凤,谭加.病理性瘢痕的发生机制与修复[J/OL].中华损伤与修复杂志(电子版),2013,8(4):347-353.
[19]周俐,石光清,邱娟.β射线照射治疗增生性瘢痕患者血清肿瘤坏死因子的变化及意义[J].标记免疫分析与临床,2013,20(5):315-318.
[20]李天石,曾文妮,何君君.甲壳素及其衍生物抑制瘢痕形成:研究与进展[J].中国组织工程研究,2014,18(52):8504-8508.