CAJ | 학술논문

目的研究肿瘤坏死因子-α( TNF-α)预处理对骨髓间充质干细胞( BMMSCs)表达血管细胞黏附分子-1( VCAM-1),以及移植治疗大鼠心肌梗死的影响。方法第3~5代大鼠BMMSCs用TNF-α(10 ng/ml)预处理24 h后,迁移黏附实验检测其体外的迁移黏附能力,Western blot检测VCAM-1的蛋白表达。 BMMSCs用DAPI标记后移植于心肌梗死大鼠的心肌内,术后4周,二维超声心动图检测大鼠左心室心功能,Masson染色检测心肌梗死区胶原沉积。实验设有未经TNF-α刺激的对照组。结果与对照组比较,TNF-α处理组BMMSCs在炎症因子TNF-α处理24 h后,体外迁移黏附力明显增强(P<0．01),黏附分子的蛋白表达水平显著升高(P<0．01)。与对照组大鼠比较,TNF-α处理组的大鼠在移植TNF-α处理的BMMSCs后,左心室射血分数明显提高( P<0．01),心肌梗死区胶原沉积明显减小。结论移植炎症因子预处理的BMMSCs明显改善大鼠的心功能及减少心肌梗死区的胶原沉积,可能与炎症因子刺激可提高BMMSCs黏附分子的表达水平有关。
목적연구종류배사인자-α( TNF-α)예처리대골수간충질간세포( BMMSCs)표체혈관세포점부분자-1( VCAM-1),이급이식치료대서심기경사적영향。방법제3~5대대서BMMSCs용TNF-α(10 ng/ml)예처리24 h후,천이점부실험검측기체외적천이점부능력,Western blot검측VCAM-1적단백표체。 BMMSCs용DAPI표기후이식우심기경사대서적심기내,술후4주,이유초성심동도검측대서좌심실심공능,Masson염색검측심기경사구효원침적。실험설유미경TNF-α자격적대조조。결과여대조조비교,TNF-α처리조BMMSCs재염증인자TNF-α처리24 h후,체외천이점부력명현증강(P<0．01),점부분자적단백표체수평현저승고(P<0．01)。여대조조대서비교,TNF-α처리조적대서재이식TNF-α처리적BMMSCs후,좌심실사혈분수명현제고( P<0．01),심기경사구효원침적명현감소。결론이식염증인자예처리적BMMSCs명현개선대서적심공능급감소심기경사구적효원침적,가능여염증인자자격가제고BMMSCs점부분자적표체수평유관。
Objective To investigate whether tumor necrosis factor-α( TNF-α) treatment could increase bone mar-row mesenchymal stem cells ( BMMSCs ) vascular cell adhesion molecule-1 ( VCAM-1 ) expression and improve post-ischemic myocardial function. Methods BMMSCs at passages 3 to 5 were treated with TNF-α for 24 h, the migration and adhesion ability of BMMSCs was measured by migration and adhesion assays in vitro, the expression of VCAM-1 was assessed by Western blot. Cells were stained with DAPI for 5 min before transplantation, at the end of the fourth week, cardiac function was examined by two-dimensional echocardiography, and collagen deposition was detected by Masson stain. Cells without treated were set as control. Results We found that compared with control group, TNF-α group significantly up-regulated the secretion of VCAM-1 after TNF-α stimulation as well as migration and adhesion ability of BMMSCs ( P<0. 01 ) , thus greatly improved post-ischemic myocardial function in rat model and decreased collagen deposition after ischemia ( P<0. 01 ) . Conclusion Treating BMMSCs with TNF-α could increase VCAM-1 expression, and improve cell-based therapies for ischemic tissue.