中国组织工程研究与临床康复
中國組織工程研究與臨床康複
중국조직공정연구여림상강복
JOURNAL OF CLINICAL REHABILITATIVE TISSUE ENGINEERING RESEARCH
2010年
18期
3343-3346
,共4页
曹正品%程春生%赵志伟%单海民
曹正品%程春生%趙誌偉%單海民
조정품%정춘생%조지위%단해민
川芎嗪%皮瓣移植%缺血再灌注损伤%自由基%中性粒细胞%内皮细胞
川芎嗪%皮瓣移植%缺血再灌註損傷%自由基%中性粒細胞%內皮細胞
천궁진%피판이식%결혈재관주손상%자유기%중성립세포%내피세포
背景:近年来研究发现,川芎嗪有清除氧自由基及保护血管内皮细胞的作用,大量的实验及临床研究涉及各种脏器,但对川芎嗪在皮瓣移植过程中缺血再灌注损伤的防治作用报道甚少.目的:观察川芎嗪对大鼠腹部皮瓣组织缺血再灌注损伤的影响,并分析其作用途径.方法:纳入24只健康SD大鼠,制备腹蹙浅动脉为蒂的轴型缺血再灌注皮瓣.按随机数字表法分为假手术组、模型对照组和川芎嗪组,每组8只.假手术组皮瓣无缺血再灌注过程:模型对照组于造模前30 min给予生理盐水4 mL/kg:川芎嗪组造模后再灌注即刻给予川芎嗪4 mL/kg腹腔注射.模型对照组及川芎嗪组在皮瓣形成即刻、缺血8 h、再灌注1 h,假手术组在皮瓣形成即刻、术后8,9 h,取皮瓣中远处组织,测定组织匀浆内超氧化物歧化酶活性及丙二醛含量,光镜及电镜下观察组织形态学变化.结果与结论:缺血8 h、再灌注1 h,模型对照组皮瓣组织中超氧化物歧化酶活性显著低于假手术组(P<0.05~0.01),川芎嗪组皮瓣组织中超氧化物歧化酶活性显著高于模型对照组(P<0.05-0.01).再灌注1 h,模型对照组皮瓣组织中丙二醛含量显著高于假手术组(P<0.01),川芎嗪组皮瓣组织中丙二醛含量显著低于模型对照组(P<0.01).与模型对照组比较,川芎嗪组皮瓣超微组织结构、血管内皮细胞损伤轻.提示川芎嗪可以抑制中性粒细胞活化、黏附,减轻组织炎症反应.保护内皮细胞,拮抗自由基的脂质过氧化,对皮瓣缺血再灌注损伤有一定的防治作用.
揹景:近年來研究髮現,川芎嗪有清除氧自由基及保護血管內皮細胞的作用,大量的實驗及臨床研究涉及各種髒器,但對川芎嗪在皮瓣移植過程中缺血再灌註損傷的防治作用報道甚少.目的:觀察川芎嗪對大鼠腹部皮瓣組織缺血再灌註損傷的影響,併分析其作用途徑.方法:納入24隻健康SD大鼠,製備腹蹙淺動脈為蒂的軸型缺血再灌註皮瓣.按隨機數字錶法分為假手術組、模型對照組和川芎嗪組,每組8隻.假手術組皮瓣無缺血再灌註過程:模型對照組于造模前30 min給予生理鹽水4 mL/kg:川芎嗪組造模後再灌註即刻給予川芎嗪4 mL/kg腹腔註射.模型對照組及川芎嗪組在皮瓣形成即刻、缺血8 h、再灌註1 h,假手術組在皮瓣形成即刻、術後8,9 h,取皮瓣中遠處組織,測定組織勻漿內超氧化物歧化酶活性及丙二醛含量,光鏡及電鏡下觀察組織形態學變化.結果與結論:缺血8 h、再灌註1 h,模型對照組皮瓣組織中超氧化物歧化酶活性顯著低于假手術組(P<0.05~0.01),川芎嗪組皮瓣組織中超氧化物歧化酶活性顯著高于模型對照組(P<0.05-0.01).再灌註1 h,模型對照組皮瓣組織中丙二醛含量顯著高于假手術組(P<0.01),川芎嗪組皮瓣組織中丙二醛含量顯著低于模型對照組(P<0.01).與模型對照組比較,川芎嗪組皮瓣超微組織結構、血管內皮細胞損傷輕.提示川芎嗪可以抑製中性粒細胞活化、黏附,減輕組織炎癥反應.保護內皮細胞,拮抗自由基的脂質過氧化,對皮瓣缺血再灌註損傷有一定的防治作用.
배경:근년래연구발현,천궁진유청제양자유기급보호혈관내피세포적작용,대량적실험급림상연구섭급각충장기,단대천궁진재피판이식과정중결혈재관주손상적방치작용보도심소.목적:관찰천궁진대대서복부피판조직결혈재관주손상적영향,병분석기작용도경.방법:납입24지건강SD대서,제비복축천동맥위체적축형결혈재관주피판.안수궤수자표법분위가수술조、모형대조조화천궁진조,매조8지.가수술조피판무결혈재관주과정:모형대조조우조모전30 min급여생리염수4 mL/kg:천궁진조조모후재관주즉각급여천궁진4 mL/kg복강주사.모형대조조급천궁진조재피판형성즉각、결혈8 h、재관주1 h,가수술조재피판형성즉각、술후8,9 h,취피판중원처조직,측정조직균장내초양화물기화매활성급병이철함량,광경급전경하관찰조직형태학변화.결과여결론:결혈8 h、재관주1 h,모형대조조피판조직중초양화물기화매활성현저저우가수술조(P<0.05~0.01),천궁진조피판조직중초양화물기화매활성현저고우모형대조조(P<0.05-0.01).재관주1 h,모형대조조피판조직중병이철함량현저고우가수술조(P<0.01),천궁진조피판조직중병이철함량현저저우모형대조조(P<0.01).여모형대조조비교,천궁진조피판초미조직결구、혈관내피세포손상경.제시천궁진가이억제중성립세포활화、점부,감경조직염증반응.보호내피세포,길항자유기적지질과양화,대피판결혈재관주손상유일정적방치작용.
BACKGROUND: Recent studies have demonstrated that ligustrazine removed oxygen-derived free radicals and protected vascular endothelial cells. Howerver, the effect of ligustrazine on skin flap ischemia-reperfusion injury was less reported. OBJECTIVE: To investigate the effect of ligustrazine on skin flap ischemia-reperfusion injury, and to analyze reaction pathway. METHODS: A total of 24 healthy SD rats were used to establish ischemia-reperfusion injured skin flap along superficial epigastric artery. All rats were randomly divided into sham-surgery, model control, and ligustrazine groups, with 8 rats per group. Ischemia-reperfusion injury was not induced in the sham-surgery group; saline (4 mL/kg) was given in the model control gorup 30 minutes prior to operation; an intraperitoneal injection of ligustrazine (4 mL/kg) was given in the ligustrazine group immediately after ischemia-reperfusion injury. Distal tissue was selected from skin flap in the model control group immediate after formation of skin flap, 8 hours after ischemia, and 1 hour after reperfusion, as well as in the sham-surgery group immediate after formation of skin flap, 8 and 9 hours after operation to measure superoxide dismutase (SOD) and malonaldehyde (MDA) contents. Histological morphology was observed under optic and electron microscopes.RESULTS AND CONCLUSION: At 8 hours after ischemia and 1 hour after reperfusion, SOD activity in the model control group was significantly less than in the sham-surgery group (P< 0.05-0.01), but the SOD activity in the ligustrazine group was significantly greater than in the model control group (P < 0.05-0.01). At 1 hour after reperfusion, MDA content in the model control group was significantly greater than sham-surgery group (P< 0.01), but the MDA content in the ligustrazine group was significantly less than in the model control group (P< 0.01). As compared with model control group, ultramicrostructure and vascular endothelial cell were mildly damaged in the ligustrazine group, suggesting that ligustrazine inhibited activation and adhesion of neutrophilic granulocytes, relieved inflammatory reaction, protected endothelial cells, resisted lipid peroxidation of free radicals, and prevented skin flap ischemia-reperfusion injury.