中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2014年
36期
5836-5841
,共6页
郑梁%吴小蔚%宋海臣%简麒超%刘迎迎%赵相宜%张黎明
鄭樑%吳小蔚%宋海臣%簡麒超%劉迎迎%趙相宜%張黎明
정량%오소위%송해신%간기초%류영영%조상의%장려명
实验动物%组织构建%白细胞介素1受体相关激酶4%皮瓣组织%缺血再灌注损伤%湖北省自然科学基金
實驗動物%組織構建%白細胞介素1受體相關激酶4%皮瓣組織%缺血再灌註損傷%湖北省自然科學基金
실험동물%조직구건%백세포개소1수체상관격매4%피판조직%결혈재관주손상%호북성자연과학기금
interleukin-1 receptor-associated kinases%surgical flaps%reperfusion injury%models,animal
背景:白细胞介素1受体相关激酶4活性引发炎症及感染的作用已得到广泛认可,但其对皮瓣缺血再灌注损伤是否有影响尚无文献报道。目的:探讨白细胞介素1受体相关激酶4活性在皮瓣缺血再灌注损伤中的意义。方法:将36只雄性SD大鼠按随机数字表法分为假手术组、缺血再灌注损伤组、白细胞介素1受体相关激酶4抑制剂组,每组12只。制备右下腹岛状皮瓣缺血再灌注损伤模型,白细胞介素1受体相关激酶4抑制剂处理组于再灌注前腹腔注射1 mL白细胞介素1受体相关激酶1/4抑制剂(100μmol/L),分别采集缺血再灌注后1,2,4,6 h的皮瓣行组织病理学观察,取缺血再灌注后1 h的皮瓣组织行白细胞介素1受体相关激酶4的蛋白表达量,并于术后7d计算皮瓣存活比例。结果与结论:组织病理学观察显示,与缺血再灌注损伤组相比,白细胞介素1受体相关激酶4抑制剂组中性粒细胞浸润及组织水肿程度明显改善,白细胞介素1受体相关激酶4的蛋白表达量逐渐降低。术后7d缺血再灌注损伤组皮瓣存活比例为(51.70±7.62)%,白细胞介素1受体相关激酶4抑制剂组皮瓣存活比例高达(86.56±12.23)%,两组比较差异有显著性意义(P<0.01)。提示大鼠皮瓣缺血再灌注损伤后,可以通过抑制白细胞介素1受体相关激酶4活化提高移植皮瓣的成活率。
揹景:白細胞介素1受體相關激酶4活性引髮炎癥及感染的作用已得到廣汎認可,但其對皮瓣缺血再灌註損傷是否有影響尚無文獻報道。目的:探討白細胞介素1受體相關激酶4活性在皮瓣缺血再灌註損傷中的意義。方法:將36隻雄性SD大鼠按隨機數字錶法分為假手術組、缺血再灌註損傷組、白細胞介素1受體相關激酶4抑製劑組,每組12隻。製備右下腹島狀皮瓣缺血再灌註損傷模型,白細胞介素1受體相關激酶4抑製劑處理組于再灌註前腹腔註射1 mL白細胞介素1受體相關激酶1/4抑製劑(100μmol/L),分彆採集缺血再灌註後1,2,4,6 h的皮瓣行組織病理學觀察,取缺血再灌註後1 h的皮瓣組織行白細胞介素1受體相關激酶4的蛋白錶達量,併于術後7d計算皮瓣存活比例。結果與結論:組織病理學觀察顯示,與缺血再灌註損傷組相比,白細胞介素1受體相關激酶4抑製劑組中性粒細胞浸潤及組織水腫程度明顯改善,白細胞介素1受體相關激酶4的蛋白錶達量逐漸降低。術後7d缺血再灌註損傷組皮瓣存活比例為(51.70±7.62)%,白細胞介素1受體相關激酶4抑製劑組皮瓣存活比例高達(86.56±12.23)%,兩組比較差異有顯著性意義(P<0.01)。提示大鼠皮瓣缺血再灌註損傷後,可以通過抑製白細胞介素1受體相關激酶4活化提高移植皮瓣的成活率。
배경:백세포개소1수체상관격매4활성인발염증급감염적작용이득도엄범인가,단기대피판결혈재관주손상시부유영향상무문헌보도。목적:탐토백세포개소1수체상관격매4활성재피판결혈재관주손상중적의의。방법:장36지웅성SD대서안수궤수자표법분위가수술조、결혈재관주손상조、백세포개소1수체상관격매4억제제조,매조12지。제비우하복도상피판결혈재관주손상모형,백세포개소1수체상관격매4억제제처리조우재관주전복강주사1 mL백세포개소1수체상관격매1/4억제제(100μmol/L),분별채집결혈재관주후1,2,4,6 h적피판행조직병이학관찰,취결혈재관주후1 h적피판조직행백세포개소1수체상관격매4적단백표체량,병우술후7d계산피판존활비례。결과여결론:조직병이학관찰현시,여결혈재관주손상조상비,백세포개소1수체상관격매4억제제조중성립세포침윤급조직수종정도명현개선,백세포개소1수체상관격매4적단백표체량축점강저。술후7d결혈재관주손상조피판존활비례위(51.70±7.62)%,백세포개소1수체상관격매4억제제조피판존활비례고체(86.56±12.23)%,량조비교차이유현저성의의(P<0.01)。제시대서피판결혈재관주손상후,가이통과억제백세포개소1수체상관격매4활화제고이식피판적성활솔。
BACKGROUND:Interleukin-1 receptor-associated kinase 4 activity-induced inflammations and infection have been extensively accepted. However, there was no report concerning its effects on flap ischemia-reperfusion injury. OBJECTIVE:To explore the significance of interleukin-1 receptor-associated kinase 4 activity in flap ischemia-reperfusion injury. METHODS:A total of 36 adult male Sprague-Dawley rats were randomized into sham-operated group (n=12), ischemia-reperfusion group (n=12) and interleukin-1 receptor-associated kinase 4 group (n=12). The models of right lower abdominal island flap ischemia-reperfusion injury were set up. Interleukin-1 receptor-associated kinase 4 group was intraperitoneal y injected with 1 mL of interleukin-1 receptor-associated kinase 4 (100μmol/L) before reperfusion. The flaps were col ected at 1, 2, 4, and 6 hours after ischemia-reperfusion injury for histopathhological observation. At 1 hour after ischemia-reperfusion, protein expression of interleukin-1 receptor-associated kinase 4 was detected in flaps. The proportion of flap survival was calculated at 7 days after surgery.RESULTS AND CONCLUSION:Histopathological observation demonstrated that compared with the ischemia-reperfusion injury group, neutrophil infiltration and edema was evidently improved, and the protein expression of interleukin-1 receptor-associated kinase 4 was gradual y reduced in the interleukin-1 receptor-associated kinase 4 group. Flap survival proportions were respectively (51.70 ±7.62)%and (86.56±12.23)%in the ischemia-reperfusion injury group and interleukin-1 receptor-associated kinase 4 group at 7 days after surgery. There were significant differences in the flap survival proportion between the two groups (P<0.01). These results showed that after flap ischemia-reperfusion injury, the inhibition of interleukin-1 receptor-associated kinase 4 activities could elevate the survival rate of transplanted flap.