CAJ | 학술논문

目的：探讨不同浓度CYP1B1抑制剂TMS（2,3’,4,5’,-四甲氧基二苯乙烯）对于C3H10T1/2多潜能干细胞脂肪分化及相关基因表达的影响。方法体外培养C3H10T1/2细胞株至完全融合后，接触抑制2 d，用激素刺激混合物（IDM）（10μg/ml胰岛素，2μmol/L地塞米松和0.5 mmol/L 3-异丁基1-甲基黄磦呤）诱导分化，同时加入不同浓度TMS（0，1.0，2.0、4.0μg/ml）。观察各组细胞分化程度，脂肪分化关键转录核因子——过氧化物酶体增殖物活化受体（PPARγ）及其下游靶基因CD36、脂肪酸结合蛋白4（FABP4）的的表达状况。结果油红和TG含量测定结果显示，CYP1B1选择性抑制剂TMS可剂量依赖地抑制IDM诱导的多潜能干细胞C3H10T1/2向脂肪细胞分化；这一作用源于TMS抑制转录核因子PPARγ的转录和蛋白表达以及下游靶基因CD36与FABP4表达。结论 TMS抑制由IDM诱导的多潜能干细胞C3H10T1/2向脂肪细胞分化。
목적：탐토불동농도CYP1B1억제제TMS（2,3’,4,5’,-사갑양기이분을희）대우C3H10T1/2다잠능간세포지방분화급상관기인표체적영향。방법체외배양C3H10T1/2세포주지완전융합후，접촉억제2 d，용격소자격혼합물（IDM）（10μg/ml이도소，2μmol/L지새미송화0.5 mmol/L 3-이정기1-갑기황표령）유도분화，동시가입불동농도TMS（0，1.0，2.0、4.0μg/ml）。관찰각조세포분화정도，지방분화관건전록핵인자——과양화물매체증식물활화수체（PPARγ）급기하유파기인CD36、지방산결합단백4（FABP4）적적표체상황。결과유홍화TG함량측정결과현시，CYP1B1선택성억제제TMS가제량의뢰지억제IDM유도적다잠능간세포C3H10T1/2향지방세포분화；저일작용원우TMS억제전록핵인자PPARγ적전록화단백표체이급하유파기인CD36여FABP4표체。결론 TMS억제유IDM유도적다잠능간세포C3H10T1/2향지방세포분화。
Objective To investigate the inhibitory effects of tetramethoxystilbene, a selective CYP1B1 inhibitor, on adipogenic differentiation of C3H10T1/2 multi-potent mesenchymal cells. Methods In vitro cultured C3H10T1/2 cells at full confluence were induced by adipogenic agents (10μg/ml insulin, 2μmol/L dexamethasone and 0.5 mmol/L 3-isobutyl-1-methylxanthine) and exposed simultaneously to TMS at the final concentrations of 1.0, 2.0 or 4.0μg/ml. Oil Red-O staining was used to observe the cell differentiation. The expression of peroxisome proliferator-activated receptor gamma (PPARγ) and its target genes cluster of differentiation 36 (CD36) and fatty acid binding protein 4 (FABP4) were quantified by real-time RT-PCR and Western blotting. Results Oil Red-O staining and TG contents revealed that TMS suppressed induced differentiation of C3H10T1/2 cells. TMS exposure of the cells dose-dependently decreased both mRNA and protein expressions of PPARγ, a key nuclear transcription factor during adipogenesis, and also lowered the mRNA expressions of PPARγ target genes CD36 and FABP4. Conclusion TMS can suppress adipogenic differentiation of C3H10T1/2 cells by inhibiting PPARγ.