中华整形外科杂志
中華整形外科雜誌
중화정형외과잡지
CHINESE JOURNAL OF PLASTIC SURGERY
2012年
6期
444-448
,共5页
简麒超%吴小蔚%宋海臣%郑梁
簡麒超%吳小蔚%宋海臣%鄭樑
간기초%오소위%송해신%정량
Toll样受体4%外科皮瓣%再灌注损伤%模型,动物
Toll樣受體4%外科皮瓣%再灌註損傷%模型,動物
Toll양수체4%외과피판%재관주손상%모형,동물
Toll-like receptor 4%Surgical flap%Reperfusion injury%Models,animal
目的 探讨Toll样受体4(Toll-like receptors 4,TLR4)在皮瓣缺血再灌注(ischmeia-reperfusion,I/R)损伤中的意义.方法 将50只雄性SD大鼠进行编号,盲视下随机分为:假手术组(10只)、I/R组(20只)、TLR4抑制剂组(20只).制备右下腹岛状皮瓣I/R模型.TLR4抑制剂组处理组于再灌注前静脉注射E5564(5 mg/kg),分别于缺血再灌注后1、2、4和6h,采用免疫组化学法检测TLR4在皮瓣组织中的表达及分布,并行组织学观察.于术后7d,应用图像分析软件计算皮瓣存活比例.应用SPSS 18.0进行统计分析,两组间比较采用F检验.结果 免疫组织化学法显示I/R组比TLR4抑制组TLR4表达明显增强,且阳性部位主要是血管壁细胞及中性粒细胞.TLR4抑制剂组再灌注后TLR4活性受到抑制,中性粒细胞浸润及组织水肿程度较I/R组明显改善.术后7 d I/R组皮瓣存活比例为(51.70 ±7.62)％,TLR4抑制剂组皮瓣存活比例明显增高,达(80.31±11.63)％,与I/R组比较差异有统计学意义(P＜0.01).结论 大鼠皮瓣缺血再灌注损伤后,皮瓣组织TLR4的表达上调中性粒细胞浸润增多.E5564能通过抑制TLR4活化,减少中性粒细胞浸润,减轻皮瓣I/R损伤.
目的 探討Toll樣受體4(Toll-like receptors 4,TLR4)在皮瓣缺血再灌註(ischmeia-reperfusion,I/R)損傷中的意義.方法 將50隻雄性SD大鼠進行編號,盲視下隨機分為:假手術組(10隻)、I/R組(20隻)、TLR4抑製劑組(20隻).製備右下腹島狀皮瓣I/R模型.TLR4抑製劑組處理組于再灌註前靜脈註射E5564(5 mg/kg),分彆于缺血再灌註後1、2、4和6h,採用免疫組化學法檢測TLR4在皮瓣組織中的錶達及分佈,併行組織學觀察.于術後7d,應用圖像分析軟件計算皮瓣存活比例.應用SPSS 18.0進行統計分析,兩組間比較採用F檢驗.結果 免疫組織化學法顯示I/R組比TLR4抑製組TLR4錶達明顯增彊,且暘性部位主要是血管壁細胞及中性粒細胞.TLR4抑製劑組再灌註後TLR4活性受到抑製,中性粒細胞浸潤及組織水腫程度較I/R組明顯改善.術後7 d I/R組皮瓣存活比例為(51.70 ±7.62)％,TLR4抑製劑組皮瓣存活比例明顯增高,達(80.31±11.63)％,與I/R組比較差異有統計學意義(P＜0.01).結論 大鼠皮瓣缺血再灌註損傷後,皮瓣組織TLR4的錶達上調中性粒細胞浸潤增多.E5564能通過抑製TLR4活化,減少中性粒細胞浸潤,減輕皮瓣I/R損傷.
목적 탐토Toll양수체4(Toll-like receptors 4,TLR4)재피판결혈재관주(ischmeia-reperfusion,I/R)손상중적의의.방법 장50지웅성SD대서진행편호,맹시하수궤분위:가수술조(10지)、I/R조(20지)、TLR4억제제조(20지).제비우하복도상피판I/R모형.TLR4억제제조처리조우재관주전정맥주사E5564(5 mg/kg),분별우결혈재관주후1、2、4화6h,채용면역조화학법검측TLR4재피판조직중적표체급분포,병행조직학관찰.우술후7d,응용도상분석연건계산피판존활비례.응용SPSS 18.0진행통계분석,량조간비교채용F검험.결과 면역조직화학법현시I/R조비TLR4억제조TLR4표체명현증강,차양성부위주요시혈관벽세포급중성립세포.TLR4억제제조재관주후TLR4활성수도억제,중성립세포침윤급조직수종정도교I/R조명현개선.술후7 d I/R조피판존활비례위(51.70 ±7.62)％,TLR4억제제조피판존활비례명현증고,체(80.31±11.63)％,여I/R조비교차이유통계학의의(P＜0.01).결론 대서피판결혈재관주손상후,피판조직TLR4적표체상조중성립세포침윤증다.E5564능통과억제TLR4활화,감소중성립세포침윤,감경피판I/R손상.
Objective To determine the role of toll like receptor-4 signal pathways activation in ischemia-reperfusion injury of island skin flap.Methods A totol of 50 adult male SD rats were randomized into 3 groups: sham-operated group (n =10),ischemia/reperfusion group (n =20) and TLR4 inhibitor-eritoran tetrasodium (E5564)-treated group(n =20).The inguinal island skin flaps models were set up.A bolus of E5564 (5 mg/kg) was infused intravenously 60 min before reper fusionm.TLR4 binding activity in flap tissue was analyzed at 1,2,4 and 6 h of reperfusion by immunohistochemical technique and flaps were assessed histologically at 6 h of reperfusion.The viability of flaps was assessed 7 days postoperatively.Results Exprerssion TLR4 in skin flap tissue was significantly increased in I/R group,compared with E5564-treated group.Immunohistochemical exam showed TLR4 mainly expressed in skin flap vessel wall and PMN membrane.Marked neutrophil infiltration and edema was observed in I/R group,while less neutrophil infiltration was observed in E5564-treated group.In the E5564-treated group,the survival of flaps was (80.31 ± 11.63) ％,which was significantly greater than that in the I/R group(51.70 ± 7.62) ％ (P ＜ 0.01).Conclusion After ischemia-reperfusion injury in rats,the expression of TLR4 increased in the skin flap tissue with excessive neutrophil infiltration.Administration of E5564 can significantly improve flap survival by regulating the early activation of TLR4 and suppressing neutrophil infiltration within the flap.
