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
49期
8481-8487
,共7页
李晓峰%罗世兴%赵劲民%程建文%谭桢
李曉峰%囉世興%趙勁民%程建文%譚楨
리효봉%라세흥%조경민%정건문%담정
干细胞%骨髓干细胞%骨髓间充质干细胞%缺氧%凋亡%芒果苷%氯化钴%省级基金%干细胞图片文章
榦細胞%骨髓榦細胞%骨髓間充質榦細胞%缺氧%凋亡%芒果苷%氯化鈷%省級基金%榦細胞圖片文章
간세포%골수간세포%골수간충질간세포%결양%조망%망과감%록화고%성급기금%간세포도편문장
背景:缺氧性死亡限制了细胞移植和组织再生中细胞的应用。<br> 目的:观察芒果苷对氯化钴作用下骨髓间充质干细胞缺氧损伤性凋亡的保护作用。<br> 方法:体外培养大鼠骨髓间充质干细胞,应用氯化钴建立细胞缺氧模型,以芒果苷对缺氧损伤下的骨髓间充质干细胞进行保护,通过MTT实验观察芒果苷对大鼠骨髓间充质干细胞缺氧损伤的保护作用;采用流式细胞仪检测芒果苷对大鼠骨髓间充质干细胞缺氧保护的细胞凋亡及线粒体膜电位检测结果。<br> 结果与结论:氯化钴能显著抑制大鼠骨髓间充质干细胞的生长,并且呈明显的剂量依赖关系。氯化钴200μmol/L处理细胞12 h,诱导细胞凋亡率为(42.49±3.96)%;处理细胞24 h,诱导细胞凋亡率为(46.37±4.49)%,随着芒果苷浓度的增加,大鼠骨髓间充质干细胞缺氧损伤的凋亡率逐步减少(P<0.01),芒果苷对大鼠骨髓间充质干细胞缺氧损伤具有保护作用,且呈浓度依赖性。结果提示,氯化钴缺氧模型能成功诱导大鼠骨髓间充质干细胞凋亡,具有剂量准确可控、无特殊设备要求、易操作等优点;芒果苷能有效抑制缺氧损伤时骨髓间充质干细胞的凋亡,对细胞具有保护作用。
揹景:缺氧性死亡限製瞭細胞移植和組織再生中細胞的應用。<br> 目的:觀察芒果苷對氯化鈷作用下骨髓間充質榦細胞缺氧損傷性凋亡的保護作用。<br> 方法:體外培養大鼠骨髓間充質榦細胞,應用氯化鈷建立細胞缺氧模型,以芒果苷對缺氧損傷下的骨髓間充質榦細胞進行保護,通過MTT實驗觀察芒果苷對大鼠骨髓間充質榦細胞缺氧損傷的保護作用;採用流式細胞儀檢測芒果苷對大鼠骨髓間充質榦細胞缺氧保護的細胞凋亡及線粒體膜電位檢測結果。<br> 結果與結論:氯化鈷能顯著抑製大鼠骨髓間充質榦細胞的生長,併且呈明顯的劑量依賴關繫。氯化鈷200μmol/L處理細胞12 h,誘導細胞凋亡率為(42.49±3.96)%;處理細胞24 h,誘導細胞凋亡率為(46.37±4.49)%,隨著芒果苷濃度的增加,大鼠骨髓間充質榦細胞缺氧損傷的凋亡率逐步減少(P<0.01),芒果苷對大鼠骨髓間充質榦細胞缺氧損傷具有保護作用,且呈濃度依賴性。結果提示,氯化鈷缺氧模型能成功誘導大鼠骨髓間充質榦細胞凋亡,具有劑量準確可控、無特殊設備要求、易操作等優點;芒果苷能有效抑製缺氧損傷時骨髓間充質榦細胞的凋亡,對細胞具有保護作用。
배경:결양성사망한제료세포이식화조직재생중세포적응용。<br> 목적:관찰망과감대록화고작용하골수간충질간세포결양손상성조망적보호작용。<br> 방법:체외배양대서골수간충질간세포,응용록화고건립세포결양모형,이망과감대결양손상하적골수간충질간세포진행보호,통과MTT실험관찰망과감대대서골수간충질간세포결양손상적보호작용;채용류식세포의검측망과감대대서골수간충질간세포결양보호적세포조망급선립체막전위검측결과。<br> 결과여결론:록화고능현저억제대서골수간충질간세포적생장,병차정명현적제량의뢰관계。록화고200μmol/L처리세포12 h,유도세포조망솔위(42.49±3.96)%;처리세포24 h,유도세포조망솔위(46.37±4.49)%,수착망과감농도적증가,대서골수간충질간세포결양손상적조망솔축보감소(P<0.01),망과감대대서골수간충질간세포결양손상구유보호작용,차정농도의뢰성。결과제시,록화고결양모형능성공유도대서골수간충질간세포조망,구유제량준학가공、무특수설비요구、역조작등우점;망과감능유효억제결양손상시골수간충질간세포적조망,대세포구유보호작용。
BACKGROUND:Hypoxic death limits application of cells in transplantation and tissue regeneration. <br> OBJECTIVE:To investigate the protective effects of mangiferin on bone marrow-derived mesenchymal stem cells against hypoxia injury-induced apoptosis resulted from cobalt chloride. <br> METHODS:Rat bone marrow-derived mesenchymal stem cells were in vitro cultured and hypoxia cellmodel was established by cobalt chloride. Model cells were treated with mangiferin. Protective effects of mangiferin were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide;cellapoptosis and mitochondrial membrane potential were detected using flow cytometry. <br> RESULTS AND CONCLUSION:Cobalt chloride significantly inhibited growth of bone marrow-derived mesenchymal stem cells in a dose-dependent manner. The apoptosis rate of cells was (42.49±3.96)%after treated with 200μmol/L cobalt chloride for 12 hours, (46.37±4.49)%after treated for 24 hours. With increasing concentration of mangiferin, apoptosis of bone marrow-derived mesenchymal stem cells in hypoxic model was gradual y reduced (P<0.01), indicating that mangiferin has a protective effect in a concentration-dependent manner on rat bone marrow-derived mesenchymal stem cells in hypoxic injury. Cobalt chloride can induce hypoxic model successful y in bone marrow-derived mesenchymal stem cells. There are some advantages of accurate dose control, no special equipment requirements, and easy operation. Mangiferin can effectively inhibit bone marrow-derived mesenchymal stem cells apoptosis under hypoxic injury.