中华整形外科杂志
中華整形外科雜誌
중화정형외과잡지
CHINESE JOURNAL OF PLASTIC SURGERY
2008年
6期
475-477
,共3页
陈蕊%傅敏刚%陆毅%王琳%平萍%范志宏
陳蕊%傅敏剛%陸毅%王琳%平萍%範誌宏
진예%부민강%륙의%왕림%평평%범지굉
瘢痕%成纤维细胞%黏着斑激酶%寡核苷酸,反义%胶原
瘢痕%成纖維細胞%黏著斑激酶%寡覈苷痠,反義%膠原
반흔%성섬유세포%점착반격매%과핵감산,반의%효원
Scars%Fibroblasts%FAK%Oligonucleotides,antisense%Collagen
目的 研究黏着斑激酶(focal adhesion kinase,FAK)在人增生性瘢痕发病机制中的作用.方法 体外分离、培养人增生性瘢痕成纤维细胞(hyperthrophic scar fibroblasts,HSFB).在脂质体介导下将FAK反义寡核苷酸转染至HSFB中设为FAK反义寡核苷酸治疗组(AT组),仅加入脂质体为脂质体对照组(LPC组),不加脂质体和反义寡核苷酸为空白对照组(LC组).通过荧光定量PCR方法 检测HSFB细胞中FAK mRNA指数,采用3H-脯氨酸掺入法测定HSFB细胞的胶原合成量.结果 转染48 h后,AT组FAKmRNA值为0.043±0.030,明显低于LC组(0.124±0.070)及LPC组(0.127±0.0195,P＜0.05).AT组的3H-脯氨酸掺入率为257.0±15.14,低于LC组(962.2±300.5)及LPC组(930.8±28.97,P＜0.01).结论 FAK反义寡核苷酸能抑制体外培养的HSFB中FAK基因的表达和胶原合成,FAK在人增生性瘢痕的发病中发挥了一定作用.
目的 研究黏著斑激酶(focal adhesion kinase,FAK)在人增生性瘢痕髮病機製中的作用.方法 體外分離、培養人增生性瘢痕成纖維細胞(hyperthrophic scar fibroblasts,HSFB).在脂質體介導下將FAK反義寡覈苷痠轉染至HSFB中設為FAK反義寡覈苷痠治療組(AT組),僅加入脂質體為脂質體對照組(LPC組),不加脂質體和反義寡覈苷痠為空白對照組(LC組).通過熒光定量PCR方法 檢測HSFB細胞中FAK mRNA指數,採用3H-脯氨痠摻入法測定HSFB細胞的膠原閤成量.結果 轉染48 h後,AT組FAKmRNA值為0.043±0.030,明顯低于LC組(0.124±0.070)及LPC組(0.127±0.0195,P＜0.05).AT組的3H-脯氨痠摻入率為257.0±15.14,低于LC組(962.2±300.5)及LPC組(930.8±28.97,P＜0.01).結論 FAK反義寡覈苷痠能抑製體外培養的HSFB中FAK基因的錶達和膠原閤成,FAK在人增生性瘢痕的髮病中髮揮瞭一定作用.
목적 연구점착반격매(focal adhesion kinase,FAK)재인증생성반흔발병궤제중적작용.방법 체외분리、배양인증생성반흔성섬유세포(hyperthrophic scar fibroblasts,HSFB).재지질체개도하장FAK반의과핵감산전염지HSFB중설위FAK반의과핵감산치료조(AT조),부가입지질체위지질체대조조(LPC조),불가지질체화반의과핵감산위공백대조조(LC조).통과형광정량PCR방법 검측HSFB세포중FAK mRNA지수,채용3H-포안산참입법측정HSFB세포적효원합성량.결과 전염48 h후,AT조FAKmRNA치위0.043±0.030,명현저우LC조(0.124±0.070)급LPC조(0.127±0.0195,P＜0.05).AT조적3H-포안산참입솔위257.0±15.14,저우LC조(962.2±300.5)급LPC조(930.8±28.97,P＜0.01).결론 FAK반의과핵감산능억제체외배양적HSFB중FAK기인적표체화효원합성,FAK재인증생성반흔적발병중발휘료일정작용.
Objective To study the role of focal adhesion kinase(FAK) in the pathogenesis of human hyperthrophic scar.Methods Human hyperthrophic scar flbroblasts (HSFB) were isolated from human hypertrophic scar and cultured in vitro.The cells were then divided into 3 groups as AT group(phosphorethioate FAK ASODN was transfectod into the HSFB by liposome),I.PC group( liposeme only),and LC group( control group,without liposome or ASODN).The FAKmRNA index of HSFB was assessed by polymerase chain reaction method( FQ-PCR).The collagen sythesis of HSFB was assessed by 3 H-proline incorporation method.Results The FAK mRNA index of HSFB in AT group 48 hours after trasfection was significantly lower than that in LPC and LC groups (0.043±0.030,0.124±0.070,0.127±0.0195,P＜0.05 ).The 3 H-proline incorporation rote in AT group was lower than that in LPC and LC groups(257.0±15.14,962.2±300.5,930.8±28.97,P ＜0.01).Conclusion The expression of FAK gene and collagen synthesis of the cultured HSFB could be inhibited by FAK ASODN,indicating that FAK played a role in the development of excessive fibrosis of human hypertrophic scar.
