CAJ | 학술논문

目的研究吡格列酮对成骨细胞增殖及凋亡的影响,并进一步了解其凋亡发生机制.方法以MC3T3-E1成骨细胞株为实验对象,分别用0、5、10、20、30、40 μmol/L吡格列酮干预,观察细胞活性、细胞周期及凋亡率的变化,同时检测细胞Bcl-2,Bax蛋白表达.结果随着浓度增加,成骨细胞的活性逐渐降低;与对照组相比,G0/G1,G2/M期细胞增多,S期细胞明显减少;凋亡率在5、10 μmol/L时低于对照组,30、40 μmol/L较对照组显著增高;Bax表达在10 μmol/L时明显减弱,20 μmol/L时回复到正常,30、40μmol/L较对照组显著增强;Bcl-2表达在浓度≤20 μmol/L时显著增强;对于Bax/Bcl-2相对表达强度与细胞凋亡率做相关性分析,两者呈显著性正相关(n=15,r=0.796,P＜0.01).结论吡格列酮在低浓度抑制成骨细胞凋亡,对细胞起保护作用,较高浓度则促进细胞凋亡,Bax/Bcl-2参与其凋亡机制,并可能起关键调控作用.吡格列酮抑制成骨细胞DNA合成,抑制细胞增殖,导致细胞活性下降.
목적 연구필격렬동대성골세포증식급조망적영향,병진일보료해기조망발생궤제.방법 이MC3T3-E1성골세포주위실험대상,분별용0、5、10、20、30、40 μmol/L필격렬동간예,관찰세포활성、세포주기급조망솔적변화,동시검측세포Bcl-2,Bax단백표체.결과 수착농도증가,성골세포적활성축점강저;여대조조상비,G0/G1,G2/M기세포증다,S기세포명현감소;조망솔재5、10 μmol/L시저우대조조,30、40 μmol/L교대조조현저증고;Bax표체재10 μmol/L시명현감약,20 μmol/L시회복도정상,30、40μmol/L교대조조현저증강;Bcl-2표체재농도≤20 μmol/L시현저증강;대우Bax/Bcl-2상대표체강도여세포조망솔주상관성분석,량자정현저성정상관(n=15,r=0.796,P＜0.01).결론 필격렬동재저농도억제성골세포조망,대세포기보호작용,교고농도칙촉진세포조망,Bax/Bcl-2삼여기조망궤제,병가능기관건조공작용.필격렬동억제성골세포DNA합성,억제세포증식,도치세포활성하강.
Objective To investigate the effects of pioglitazone on osteoblast proliferation and apoptosis.Methods MC3T3-E1 mouse osteoblastic cells were treated with 0, 5, 10, 20, 30, and 40 μmol/L pioglitazone for 24 h. Cell viability was measured by MTT, cell cycle and apoptosis were inspected with flow cytometry, the expressions of Bcl-2 and Bax proteins were examined via immuno-chemical staining. Results Survival of osteoblasts decreased in a dose-dependent manner. Compared with the control group, the cells in the G0/G1 and G2/M stages increased, while the cells in S stage decreased significantly. The percentage of apoptosis at 5 and 10 μmol/L were lower than that of the control group(P ＜ 0.05), While it was increased significantly at 30 and 40 μmol/L(P ＜0.01). Bax expression was attenuated at 10 μmol/L(P＜0. 01), returned to normal by 20 μmol/L, and was increased by 30 and 40 μmol/L(P ＜ 0. 01). Bcl-2 expression was enhanced at the dose ≤ 20 μmol/L(P ＜0.01). Positive correlation was found between the death rate and the expression intensity of Bax/Bcl-2(n = 15, r=0.796, P＜0.01). Conclusions Pioglitazone inhibits apoptosis of osteoblasts at low concentrations and protects the cells, but promotes their apoptosis at higher concentration, Bax/Bcl-2 may play an important role in mediating the piglitazone-induced apoptosis of osteoblasts. It inhibits DNA synthesis and cell proliferation.