中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2013年
7期
1220-1227
,共8页
侯传举%齐岩梅%张端珍%王琦光%崔春生%匡丽%陈兵
侯傳舉%齊巖梅%張耑珍%王琦光%崔春生%劻麗%陳兵
후전거%제암매%장단진%왕기광%최춘생%광려%진병
组织构建%组织构建与生物活性因子%心肌细胞%心脏成纤维细胞%基质细胞衍生因子 1α%物理损伤%先天性心脏缺损%房间隔缺损%室间隔缺损%动脉导管未闭%增殖%趋化%国家自然科学基金%组织构建图片文章
組織構建%組織構建與生物活性因子%心肌細胞%心髒成纖維細胞%基質細胞衍生因子 1α%物理損傷%先天性心髒缺損%房間隔缺損%室間隔缺損%動脈導管未閉%增殖%趨化%國傢自然科學基金%組織構建圖片文章
조직구건%조직구건여생물활성인자%심기세포%심장성섬유세포%기질세포연생인자 1α%물리손상%선천성심장결손%방간격결손%실간격결손%동맥도관미폐%증식%추화%국가자연과학기금%조직구건도편문장
背景:在心脏缺损边缘造成新创面能够促进缺损自愈,基质细胞衍生因子1α能够促进血管生成以及心脏功能.目的:探讨物理损伤及基质细胞衍生因子1α对心肌细胞增殖的影响及心肌细胞对心脏成纤维细胞迁移的趋化作用.方法:原代分离培养大鼠心肌细胞和心脏成纤维细胞,采用刮伤法建立物理损伤模型,并应用10-160μg/L 的基质细胞衍生因子1α进行干预;CCK-8法检测心肌细胞的增殖能力;Transwel 法检测心肌细胞趋化下心脏成纤维细胞的迁移能力.结果与结论:不同浓度的基质细胞衍生因子1α均可提高物理损伤下心肌细胞的增殖能力,尤以80μg/L基质细胞衍生因子1α作用下心肌细胞增殖最明显.同时,物理损伤联合基质细胞衍生因子1α培养的心肌细胞可显著增加心脏成纤维细胞的迁移能力,并且随着趋化培养时间的延长,迁移能力增加更明显.可见基质细胞衍生因子1α能提高物理损伤心肌细胞的增殖能力,物理损伤联合基质细胞衍生因子1α培养的心肌细胞对心脏成纤维细胞的迁移具有促进作用.
揹景:在心髒缺損邊緣造成新創麵能夠促進缺損自愈,基質細胞衍生因子1α能夠促進血管生成以及心髒功能.目的:探討物理損傷及基質細胞衍生因子1α對心肌細胞增殖的影響及心肌細胞對心髒成纖維細胞遷移的趨化作用.方法:原代分離培養大鼠心肌細胞和心髒成纖維細胞,採用颳傷法建立物理損傷模型,併應用10-160μg/L 的基質細胞衍生因子1α進行榦預;CCK-8法檢測心肌細胞的增殖能力;Transwel 法檢測心肌細胞趨化下心髒成纖維細胞的遷移能力.結果與結論:不同濃度的基質細胞衍生因子1α均可提高物理損傷下心肌細胞的增殖能力,尤以80μg/L基質細胞衍生因子1α作用下心肌細胞增殖最明顯.同時,物理損傷聯閤基質細胞衍生因子1α培養的心肌細胞可顯著增加心髒成纖維細胞的遷移能力,併且隨著趨化培養時間的延長,遷移能力增加更明顯.可見基質細胞衍生因子1α能提高物理損傷心肌細胞的增殖能力,物理損傷聯閤基質細胞衍生因子1α培養的心肌細胞對心髒成纖維細胞的遷移具有促進作用.
배경:재심장결손변연조성신창면능구촉진결손자유,기질세포연생인자1α능구촉진혈관생성이급심장공능.목적:탐토물리손상급기질세포연생인자1α대심기세포증식적영향급심기세포대심장성섬유세포천이적추화작용.방법:원대분리배양대서심기세포화심장성섬유세포,채용괄상법건립물리손상모형,병응용10-160μg/L 적기질세포연생인자1α진행간예;CCK-8법검측심기세포적증식능력;Transwel 법검측심기세포추화하심장성섬유세포적천이능력.결과여결론:불동농도적기질세포연생인자1α균가제고물리손상하심기세포적증식능력,우이80μg/L기질세포연생인자1α작용하심기세포증식최명현.동시,물리손상연합기질세포연생인자1α배양적심기세포가현저증가심장성섬유세포적천이능력,병차수착추화배양시간적연장,천이능력증가경명현.가견기질세포연생인자1α능제고물리손상심기세포적증식능력,물리손상연합기질세포연생인자1α배양적심기세포대심장성섬유세포적천이구유촉진작용.
BACKGROUND: New wound in the border of defected hearts can promote self-healing, and stromal cel -derived factor-1 alpha can promote angiogenesis and cardiac function. OBJECTIVE: To investigate the effects of mechanical injury and stromal cel -derived factor-1 alpha on the proliferation of cardiomyocytes and the effects of cardiomyocytes on chemotactic migration of cardiac fibroblasts. METHODS: Rat cardiomyocytes and cardiac fibroblasts were cultured primarily. Rat cardiomyocytes were injured mechanical y by scratching, and treated with 10-160 μg/L stromal cel -derived factor-1 alpha. The Cel Counting Kit-8 assay was employed to evaluate the proliferation of cardiomyocytes and the Transwel migration assay was used to detect the chemotaxis and migration capability of cardiac fibroblasts. RESULTS AND CONCLUSION: Under mechanical injury condition, stromal cel -derived factor-1 alpha significantly promoted the growth of cardiomyocytes with the maximum effect occurring at 80 μg/L. In addition, mechanical y injured and stromal cel -derived factor-1 alpha cultured cardiomyocytes remarkably promoted the migration of cardiac fibroblasts in a time-dependent fashion. These findings indicate that stromal cel -derived factor-1 alpha could promote the growth of cardiomyocytes under mechanical injury condition; otherwise, mechanical y injured and stromal cel -derived factor-1 alpha cultured cardiomyocytes could promote the migration of cardiac fibroblasts.