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
41期
7205-7212
,共8页
仲兴%张德志%韩鸿宾%李凯%杨智洋%付文举
仲興%張德誌%韓鴻賓%李凱%楊智洋%付文舉
중흥%장덕지%한홍빈%리개%양지양%부문거
组织构建%骨组织构建%蛋白激酶C途径%成骨细胞%地塞米松%凋亡%糖皮质激素
組織構建%骨組織構建%蛋白激酶C途徑%成骨細胞%地塞米鬆%凋亡%糖皮質激素
조직구건%골조직구건%단백격매C도경%성골세포%지새미송%조망%당피질격소
osteoblasts%dexamethasone%bone and bones%protein kinase C%pherbols%mechanotrasduction,cellular
背景：地塞米松以增加细胞周期时间的方法提高细胞凋亡来减少成骨细胞和骨细胞的数量。蛋白激酶C是细胞内信号传导通路的一种，与细胞凋亡有关已有相关文献报道。目的：探讨地塞米松诱导成骨细胞凋亡在蛋白激酶C细胞内信号转导途径方向的机制。方法：取胎鼠骨髓间充质干细胞进行成骨诱导，分为塞米松模型组、佛波醇组和星型胞菌素组。地塞米松模型组加入1×10-6 mol/L地塞米松，佛波醇组加入1×10-6 mol/L地塞米松和1×10-7 mol/L佛波醇，星型胞菌素组加入1×10-6 mol/L地塞米松和1×10-7结果与结论：地塞米松可明显的诱导凋亡，加入佛波醇后凋亡明显增加，加入星形孢菌素后凋亡明显减少。加入地塞米松后胞浆的蛋白激酶C明显减少，包膜明显增加。加入地塞米松不同时间，胞浆和胞膜的蛋白激酶C变化在30 min最明显。说明地塞米松诱导成骨细胞凋亡的机制与蛋白激酶C有关，地塞米松为蛋白激酶C激动剂。细胞受到刺激后，胞浆的蛋白激酶C转移至包膜，胞浆中的蛋白激酶C量减少，包膜中的增加。mol/L星型胞菌素，观察不同干预组细胞的增殖或抑制，并对细胞膜及细胞质中蛋白激酶C含量的变化进行检测。
揹景：地塞米鬆以增加細胞週期時間的方法提高細胞凋亡來減少成骨細胞和骨細胞的數量。蛋白激酶C是細胞內信號傳導通路的一種，與細胞凋亡有關已有相關文獻報道。目的：探討地塞米鬆誘導成骨細胞凋亡在蛋白激酶C細胞內信號轉導途徑方嚮的機製。方法：取胎鼠骨髓間充質榦細胞進行成骨誘導，分為塞米鬆模型組、彿波醇組和星型胞菌素組。地塞米鬆模型組加入1×10-6 mol/L地塞米鬆，彿波醇組加入1×10-6 mol/L地塞米鬆和1×10-7 mol/L彿波醇，星型胞菌素組加入1×10-6 mol/L地塞米鬆和1×10-7結果與結論：地塞米鬆可明顯的誘導凋亡，加入彿波醇後凋亡明顯增加，加入星形孢菌素後凋亡明顯減少。加入地塞米鬆後胞漿的蛋白激酶C明顯減少，包膜明顯增加。加入地塞米鬆不同時間，胞漿和胞膜的蛋白激酶C變化在30 min最明顯。說明地塞米鬆誘導成骨細胞凋亡的機製與蛋白激酶C有關，地塞米鬆為蛋白激酶C激動劑。細胞受到刺激後，胞漿的蛋白激酶C轉移至包膜，胞漿中的蛋白激酶C量減少，包膜中的增加。mol/L星型胞菌素，觀察不同榦預組細胞的增殖或抑製，併對細胞膜及細胞質中蛋白激酶C含量的變化進行檢測。
배경：지새미송이증가세포주기시간적방법제고세포조망래감소성골세포화골세포적수량。단백격매C시세포내신호전도통로적일충，여세포조망유관이유상관문헌보도。목적：탐토지새미송유도성골세포조망재단백격매C세포내신호전도도경방향적궤제。방법：취태서골수간충질간세포진행성골유도，분위새미송모형조、불파순조화성형포균소조。지새미송모형조가입1×10-6 mol/L지새미송，불파순조가입1×10-6 mol/L지새미송화1×10-7 mol/L불파순，성형포균소조가입1×10-6 mol/L지새미송화1×10-7결과여결론：지새미송가명현적유도조망，가입불파순후조망명현증가，가입성형포균소후조망명현감소。가입지새미송후포장적단백격매C명현감소，포막명현증가。가입지새미송불동시간，포장화포막적단백격매C변화재30 min최명현。설명지새미송유도성골세포조망적궤제여단백격매C유관，지새미송위단백격매C격동제。세포수도자격후，포장적단백격매C전이지포막，포장중적단백격매C량감소，포막중적증가。mol/L성형포균소，관찰불동간예조세포적증식혹억제，병대세포막급세포질중단백격매C함량적변화진행검측。
BACKGROUND:Dexamethasone can improve the cellapoptosis and decrease the number of osteoblasts and bone cells through increasing the time of cellcycle. Protein kinase C is a kind of intraecellular singnal transduction pathways, and there are related reports on the relationship between protein kinase C and cellapoptosis. OBJECTIVE:To investigate the mechanism of dexamethasone-induced osteoblast apoptosis via protein kinase C intracellular signal transduction pathway. METHODS:Fetal rat bone marrow mesenchymal stem cells were col ected for osteogenic induction, and the cells were divided into dexamethasone group, phorbol group and star cytochalasin group. The cells in the dexamethasone group were added with 1×10-6 mol/L dexamethasone, the cells in the phorbol group were added with 1×10-6 mol/L dexamethasone and 1×10-7 mol/L phorbol, while the cells in the star cytochalasin group were added with 1×10-6 mol/L dexamethasone and 1×10-7 RESULTS AND CONCLUSION:Dexamethasone could induce apoptosis significantly, and after added with mol/L star cytochalasin. The proliferation and inhibition of the cells in different intervention groups were observed, and the content of protein kinase C in the cellmembrane and cytoplasm was measured. phorbol, the apoptosis was increased significantly;while after added with star cytochalasin, the apoptosis was decreased significantly. After added with dexamethasone, the content of protein kinase C in the cytoplasm was significantly decreased, while increased in the cellmembrane. At different time points after added with dexamethasone, the change of the content of protein kinase C in the cytoplasm and cellmembrane was most significant at 30 minutes. The results indicated that mechanism of dexamethasone-induced osteoblast apoptosis was correlated with protein kinase C, and dexamethasone was the agonist of protein kinase C. After the cells were stimulated, the protein kinase C in the cytoplasm wil moved to the cellmembrane, and then the content of protein kinase C in the cytoplasm was decreased, while increased in the cellmembrane.
