天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2013年
10期
981-984
,共4页
关晓慧%王君%郭菲%周杰%王宝利
關曉慧%王君%郭菲%週傑%王寶利
관효혜%왕군%곽비%주걸%왕보리
脂细胞%细胞分化%骨化三醇%PPARγ%CCAAT增强子结合蛋白α%β连环素%脂肪细胞表征因子aP2
脂細胞%細胞分化%骨化三醇%PPARγ%CCAAT增彊子結閤蛋白α%β連環素%脂肪細胞錶徵因子aP2
지세포%세포분화%골화삼순%PPARγ%CCAAT증강자결합단백α%β련배소%지방세포표정인자aP2
adipocytes%cell differentiation%calcitriol%PPAR gamma%CCAAT-enhancer-binding protein-alpha%beta catenin%adipocyte characterization factor aP2
目的研究1,25-二羟基维生素D3[1,25(OH)2D3]对脂肪细胞分化的影响及其机制。方法以间充质干细胞系C3H10T1/2为研究对象,将其分为6组,分别为对照组、诱导分化组和4个不同剂量的1,25(OH)2D3处理组。其中对照组加入溶媒,诱导分化组加入脂肪细胞诱导分化试剂,1,25(OH)2D3处理组除了加入脂肪细胞诱导分化试剂外,予以10-9、10-8、10-7、10-6 mol/L 1,25(OH)2D3处理。处理后5 d进行油红O染色,RT-PCR检测脂肪细胞特异性转录因子和Wnt/β-catenin信号通路相关因子表达水平,Western blot检测β-catenin蛋白水平。结果1,25(OH)2D3能够强烈抑制脂肪细胞生成,阻断脂肪细胞特异性转录因子过氧化物酶体增殖物激活受体(PPAR)γ、CCAAT增强子结合蛋白(C/EBP)α及脂肪细胞表征因子aP2 mRNA表达,下调Wnt/β-catenin信号通路抑制因子分泌性卷曲相关蛋白1(sFRP1)mRNA,上调β连环素(β-catenin)蛋白水平。结论1,25(OH)2D3强烈抑制脂肪细胞分化,该作用可能与其激活Wnt/β-catenin信号通路有关。
目的研究1,25-二羥基維生素D3[1,25(OH)2D3]對脂肪細胞分化的影響及其機製。方法以間充質榦細胞繫C3H10T1/2為研究對象,將其分為6組,分彆為對照組、誘導分化組和4箇不同劑量的1,25(OH)2D3處理組。其中對照組加入溶媒,誘導分化組加入脂肪細胞誘導分化試劑,1,25(OH)2D3處理組除瞭加入脂肪細胞誘導分化試劑外,予以10-9、10-8、10-7、10-6 mol/L 1,25(OH)2D3處理。處理後5 d進行油紅O染色,RT-PCR檢測脂肪細胞特異性轉錄因子和Wnt/β-catenin信號通路相關因子錶達水平,Western blot檢測β-catenin蛋白水平。結果1,25(OH)2D3能夠彊烈抑製脂肪細胞生成,阻斷脂肪細胞特異性轉錄因子過氧化物酶體增殖物激活受體(PPAR)γ、CCAAT增彊子結閤蛋白(C/EBP)α及脂肪細胞錶徵因子aP2 mRNA錶達,下調Wnt/β-catenin信號通路抑製因子分泌性捲麯相關蛋白1(sFRP1)mRNA,上調β連環素(β-catenin)蛋白水平。結論1,25(OH)2D3彊烈抑製脂肪細胞分化,該作用可能與其激活Wnt/β-catenin信號通路有關。
목적연구1,25-이간기유생소D3[1,25(OH)2D3]대지방세포분화적영향급기궤제。방법이간충질간세포계C3H10T1/2위연구대상,장기분위6조,분별위대조조、유도분화조화4개불동제량적1,25(OH)2D3처리조。기중대조조가입용매,유도분화조가입지방세포유도분화시제,1,25(OH)2D3처리조제료가입지방세포유도분화시제외,여이10-9、10-8、10-7、10-6 mol/L 1,25(OH)2D3처리。처리후5 d진행유홍O염색,RT-PCR검측지방세포특이성전록인자화Wnt/β-catenin신호통로상관인자표체수평,Western blot검측β-catenin단백수평。결과1,25(OH)2D3능구강렬억제지방세포생성,조단지방세포특이성전록인자과양화물매체증식물격활수체(PPAR)γ、CCAAT증강자결합단백(C/EBP)α급지방세포표정인자aP2 mRNA표체,하조Wnt/β-catenin신호통로억제인자분비성권곡상관단백1(sFRP1)mRNA,상조β련배소(β-catenin)단백수평。결론1,25(OH)2D3강렬억제지방세포분화,해작용가능여기격활Wnt/β-catenin신호통로유관。
Objective To investigate the effect of 1, 25-dihydroxy-vitamin D3 (1, 25 (OH)2D3) on adipocyte differen-tiation and the underlying mechanism. Methods The mesenchymal stem cell line C3H10T1/2 was randomly divided into 6 groups including control group, differentiation group and 4 different doses of 1, 25(OH)2D3 groups. The control group was treated with vehicle. The differentiation group was supplemented with adipocyte differentiation reagent. And the 1,25(OH)2D3 groups were treated with adipocyte differentiation reagents and 10-9, 10-8, 10-7 and 10-6 mol/L of 25(OH)2D3. After culturing for 5 days, the cells were stained with oil red O, and the expression levels of adipocyte-specific transcription factors and Wnt/β-catenin signaling pathway related genes were examined by RT-PCR or Western blot methods. Results 1,25(OH)2D3 sig-nificantly reduced the number of differentiated adipocytes and blocked the mRNA levels of adipocyte specific transcription factor PPARγ(peroxisome proliferator-activated receptor gamma), C/EBPα(CCAAT enhancer binding proteinα) and adipo-cyte characterization factor aP2 (fatty acid binding protein 4). These were paralleled by the decreased mRNA expression of Wnt/β-catenin signaling pathway inhibitor sFRP1 (Secreted frizzled-related protein 1) and the increased level ofβ-catenin protein. Conclusion 1, 25(OH)2D3 inhibits adipocyte differentiation, which may be related to the activation of Wnt/β-catenin signaling.