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
2009年
39期
7763-7766
,共4页
莫新玲%谢福生%张建义%李全忠%夏中华%阳耀忠%潘迪华
莫新玲%謝福生%張建義%李全忠%夏中華%暘耀忠%潘迪華
막신령%사복생%장건의%리전충%하중화%양요충%반적화
冠状动脉支架置入%炎症介导素类%冠状动脉疾病%内膜增生%凋亡%血小板源性生长因子
冠狀動脈支架置入%炎癥介導素類%冠狀動脈疾病%內膜增生%凋亡%血小闆源性生長因子
관상동맥지가치입%염증개도소류%관상동맥질병%내막증생%조망%혈소판원성생장인자
目的:观察冠状动脉支架置入后患者血清中相关炎症与细胞因子水平的变化,并探讨其临床意义.方法:以"冠状动脉疾病,冠脉支架置入术,炎症介导素类,内膜增生,凋亡,血小板源性生长因子"为检索词在中国期刊全文数据库中(CNKI:1995/2008)采用电子检索方式进行文献初检,语种限定为中文.收集与冠状动脉支架置入后相关炎症、细胞因子水平的变化及其意义相关文献17篇,从冠心病并置入冠状动脉支架的研究对象、实验分组、标本采集、测定方法、实验结果、实验结论加以整理,同时对置入冠状动脉支架的冠心病患者进行基本的分析,结合支架置入后的相关炎症与细胞因子水平的变化,并探讨其临床意义.结果:17篇有关冠心病患者冠状动脉支架置入后的文献均显示,患者血清中相关炎症与细胞因子水平呈动态变化,其可能的机制有:①球囊扩张或支架置入不可避免地损伤内皮细胞,内皮受损、脱落、胶原暴露,可引发或促进斑块破裂,使斑块中的炎症递质或细胞因子促炎因素暴露于血循环中,使循环血中性粒细胞激活,并上调白细胞勃附分子CD11b的表达和激活.②多种刺激可以诱发核转录因子介导的炎性反应,产生白细胞介素6,刺激肝细胞产生C-反应蛋白.③支架置入后仅数天血管紧张素Ⅱ水平较置入前升高,并且随着时间的推移有增高趋势,同时通过血小板源性生长因子调节增殖;通过诱导内皮素的基因表达,使内皮素合成增加等共同作用,促进血管平滑肌细胞的增殖与迁移,从而促进动脉粥样硬化形成,且与球囊损伤有关,可能是再狭窄的机制之一.结论:相关炎症与细胞因子水平的变化可作为冠状动脉支架置入后炎症反应强弱的指标;可溶性cD40配体、C-反应蛋白、基质金属蛋白酶9可能与支架内再狭窄有关.
目的:觀察冠狀動脈支架置入後患者血清中相關炎癥與細胞因子水平的變化,併探討其臨床意義.方法:以"冠狀動脈疾病,冠脈支架置入術,炎癥介導素類,內膜增生,凋亡,血小闆源性生長因子"為檢索詞在中國期刊全文數據庫中(CNKI:1995/2008)採用電子檢索方式進行文獻初檢,語種限定為中文.收集與冠狀動脈支架置入後相關炎癥、細胞因子水平的變化及其意義相關文獻17篇,從冠心病併置入冠狀動脈支架的研究對象、實驗分組、標本採集、測定方法、實驗結果、實驗結論加以整理,同時對置入冠狀動脈支架的冠心病患者進行基本的分析,結閤支架置入後的相關炎癥與細胞因子水平的變化,併探討其臨床意義.結果:17篇有關冠心病患者冠狀動脈支架置入後的文獻均顯示,患者血清中相關炎癥與細胞因子水平呈動態變化,其可能的機製有:①毬囊擴張或支架置入不可避免地損傷內皮細胞,內皮受損、脫落、膠原暴露,可引髮或促進斑塊破裂,使斑塊中的炎癥遞質或細胞因子促炎因素暴露于血循環中,使循環血中性粒細胞激活,併上調白細胞勃附分子CD11b的錶達和激活.②多種刺激可以誘髮覈轉錄因子介導的炎性反應,產生白細胞介素6,刺激肝細胞產生C-反應蛋白.③支架置入後僅數天血管緊張素Ⅱ水平較置入前升高,併且隨著時間的推移有增高趨勢,同時通過血小闆源性生長因子調節增殖;通過誘導內皮素的基因錶達,使內皮素閤成增加等共同作用,促進血管平滑肌細胞的增殖與遷移,從而促進動脈粥樣硬化形成,且與毬囊損傷有關,可能是再狹窄的機製之一.結論:相關炎癥與細胞因子水平的變化可作為冠狀動脈支架置入後炎癥反應彊弱的指標;可溶性cD40配體、C-反應蛋白、基質金屬蛋白酶9可能與支架內再狹窄有關.
목적:관찰관상동맥지가치입후환자혈청중상관염증여세포인자수평적변화,병탐토기림상의의.방법:이"관상동맥질병,관맥지가치입술,염증개도소류,내막증생,조망,혈소판원성생장인자"위검색사재중국기간전문수거고중(CNKI:1995/2008)채용전자검색방식진행문헌초검,어충한정위중문.수집여관상동맥지가치입후상관염증、세포인자수평적변화급기의의상관문헌17편,종관심병병치입관상동맥지가적연구대상、실험분조、표본채집、측정방법、실험결과、실험결론가이정리,동시대치입관상동맥지가적관심병환자진행기본적분석,결합지가치입후적상관염증여세포인자수평적변화,병탐토기림상의의.결과:17편유관관심병환자관상동맥지가치입후적문헌균현시,환자혈청중상관염증여세포인자수평정동태변화,기가능적궤제유:①구낭확장혹지가치입불가피면지손상내피세포,내피수손、탈락、효원폭로,가인발혹촉진반괴파렬,사반괴중적염증체질혹세포인자촉염인소폭로우혈순배중,사순배혈중성립세포격활,병상조백세포발부분자CD11b적표체화격활.②다충자격가이유발핵전록인자개도적염성반응,산생백세포개소6,자격간세포산생C-반응단백.③지가치입후부수천혈관긴장소Ⅱ수평교치입전승고,병차수착시간적추이유증고추세,동시통과혈소판원성생장인자조절증식;통과유도내피소적기인표체,사내피소합성증가등공동작용,촉진혈관평활기세포적증식여천이,종이촉진동맥죽양경화형성,차여구낭손상유관,가능시재협착적궤제지일.결론:상관염증여세포인자수평적변화가작위관상동맥지가치입후염증반응강약적지표;가용성cD40배체、C-반응단백、기질금속단백매9가능여지가내재협착유관.
OBJECTIVE: To observe the correlated serum inflammatory factor and cytokine changes in patients with coronary stent implantation, and to explore the significance of these changes.METHODS: Chinese Journal Full-Text Database was retrieved with search terms of coronary artery disease, percutaneous coronary interventions, inflammation, intimal hyperplasia, apoptosis and platelet-derived growth factor from 1995 to 2008. The language was restrained Chinese. A total of 17 literatures were collected, which concerns the changes of correlated inflammatory factor and cytokine levels and its significance. The literatures were sorted according to research object, experimental grouping,sample collection, assay method, experimental result, as well as experimental conclusion. Simultaneously, the patients received coronary stent implantation was analyzed to explore the significance of inflammatory factor and cytokine changes.RESULTS: The dynamic changed serum inflammatory factor and cytokine in patients with coronary stent implantation may be associated with the following mechanisms:①Endothelial cells were easily damaged in the balloon dilatation or stent implantation,therefore, inflammatory mediators or inflammatory factors were exposed to blood circulation, which stimulating neutrophilic granulocytes and up-regulating leukocyte adhesion molecule CD11b expression. ②Many stimulus could arise nuclear factor induced inflammatory reaction, produce interleukin 6, and stimulate C-reactive protein generation. ③The level of angiotensin Ⅱ increased at several days following stent implantation, and heightened with time prolonged, the proliferation of angiotensin Ⅱ was regulated by platelet-derived growth factor. By increasing the expression of endothelin, the synthesis of endothelin was accelerated, the proliferation and migration of vascular smooth muscle cells was promoted, which ultimately resulted in atherogenesis, balloon damage also involved in this process, which may be one of the mechanisms of restenosis.CONCLUSION: The changes of correlated inflammatory factor and cytokine can be served as inflammatory reaction indexes;moreover, soluble CD40 ligand, C-reactive protein and matrix metalloproteinase 9 may be associated with in-stent restenosis.