中华胰腺病杂志
中華胰腺病雜誌
중화이선병잡지
CHINESE JOURNAL OF PANCREATOLOGY
2014年
6期
385-388
,共4页
商建%邹金艳%伍威%易三凤%张海平%林军
商建%鄒金豔%伍威%易三鳳%張海平%林軍
상건%추금염%오위%역삼봉%장해평%림군
胰腺肿瘤%Hedgehog信号通路%维生素D%细胞增殖%细胞凋亡
胰腺腫瘤%Hedgehog信號通路%維生素D%細胞增殖%細胞凋亡
이선종류%Hedgehog신호통로%유생소D%세포증식%세포조망
Pancreatic neoplasms%Hedgehog signaling pathway%Vitamin D%Cell proliferation%Aplptosis
目的 探讨维生素D3抗胰腺癌的作用机制.方法 应用不同浓度的维生素D3(25、50、75、100 μmol/L)干预胰腺癌PANC1细胞,以未干预细胞作为阴性对照组.MTT比色法检测细胞的生长抑制率;流式细胞仪检测细胞的早期凋亡率;RT-PCR法检测细胞PTCH、Gli-1 mRNA的表达.结果 维生素D3呈浓度依赖性抑制PANC1细胞的增殖,以48 h点的抑制作用最强,阴性对照组及25、50、75、100 μmol/L维生素D3组的生长抑制率分别为0、16.1％、18.8％、31.8％、39.4％,组间差异有统计学意义(P值均＜0.05).阴性对照组及25、50、75、100 μmol/L维生素D3干预24 h时PANC1细胞的早期凋亡率分别为(5.89±0.57)％、(6.06±0.44)％、(16.21± 1.62)％、(16.94±0.91)％、(20.96±0.98)％,早期凋亡率随浓度的增加而增加,差异有统计学意义(P＜0.05).维生素D3干预PANC1细胞24 h后,阴性对照组及25、50、75、100 μmol/L组细胞的PTCH mRNA表达量分别为0.117±0.009、0.104 ±0.011、0.069±0.011、0.052±0.009、0.056±0.007;Gli-1 mRNA表达量分别为0.323±0.007、0.312±0.015、0.299±0.015、0.233 ±0.007、0.175 ±0.014,均随浓度的增加而下调,差异有统计学意义(P值均＜0.05).75 μmol/L维生素D3干预0、12、24、36、48 h后,PTCH mRNA表达量分别为0.142±0.008、0.127 ±0.009、0.111±0.010、0.115 ±0.003、0.102±0.007;Gli-1 mRNA分别为0.341±0.011、0.317 ±0.017、0.320±0.018、0.226 ±0.011、0.191±0.010,均随时间的延长而下调,差异有统计学意义(P值均＜0.05).结论 维生素D3可以有效抑制胰腺癌PANC1细胞的增殖,促进细胞凋亡,其机制可能与阻滞Hedgehog信号通路有关.
目的 探討維生素D3抗胰腺癌的作用機製.方法 應用不同濃度的維生素D3(25、50、75、100 μmol/L)榦預胰腺癌PANC1細胞,以未榦預細胞作為陰性對照組.MTT比色法檢測細胞的生長抑製率;流式細胞儀檢測細胞的早期凋亡率;RT-PCR法檢測細胞PTCH、Gli-1 mRNA的錶達.結果 維生素D3呈濃度依賴性抑製PANC1細胞的增殖,以48 h點的抑製作用最彊,陰性對照組及25、50、75、100 μmol/L維生素D3組的生長抑製率分彆為0、16.1％、18.8％、31.8％、39.4％,組間差異有統計學意義(P值均＜0.05).陰性對照組及25、50、75、100 μmol/L維生素D3榦預24 h時PANC1細胞的早期凋亡率分彆為(5.89±0.57)％、(6.06±0.44)％、(16.21± 1.62)％、(16.94±0.91)％、(20.96±0.98)％,早期凋亡率隨濃度的增加而增加,差異有統計學意義(P＜0.05).維生素D3榦預PANC1細胞24 h後,陰性對照組及25、50、75、100 μmol/L組細胞的PTCH mRNA錶達量分彆為0.117±0.009、0.104 ±0.011、0.069±0.011、0.052±0.009、0.056±0.007;Gli-1 mRNA錶達量分彆為0.323±0.007、0.312±0.015、0.299±0.015、0.233 ±0.007、0.175 ±0.014,均隨濃度的增加而下調,差異有統計學意義(P值均＜0.05).75 μmol/L維生素D3榦預0、12、24、36、48 h後,PTCH mRNA錶達量分彆為0.142±0.008、0.127 ±0.009、0.111±0.010、0.115 ±0.003、0.102±0.007;Gli-1 mRNA分彆為0.341±0.011、0.317 ±0.017、0.320±0.018、0.226 ±0.011、0.191±0.010,均隨時間的延長而下調,差異有統計學意義(P值均＜0.05).結論 維生素D3可以有效抑製胰腺癌PANC1細胞的增殖,促進細胞凋亡,其機製可能與阻滯Hedgehog信號通路有關.
목적 탐토유생소D3항이선암적작용궤제.방법 응용불동농도적유생소D3(25、50、75、100 μmol/L)간예이선암PANC1세포,이미간예세포작위음성대조조.MTT비색법검측세포적생장억제솔;류식세포의검측세포적조기조망솔;RT-PCR법검측세포PTCH、Gli-1 mRNA적표체.결과 유생소D3정농도의뢰성억제PANC1세포적증식,이48 h점적억제작용최강,음성대조조급25、50、75、100 μmol/L유생소D3조적생장억제솔분별위0、16.1％、18.8％、31.8％、39.4％,조간차이유통계학의의(P치균＜0.05).음성대조조급25、50、75、100 μmol/L유생소D3간예24 h시PANC1세포적조기조망솔분별위(5.89±0.57)％、(6.06±0.44)％、(16.21± 1.62)％、(16.94±0.91)％、(20.96±0.98)％,조기조망솔수농도적증가이증가,차이유통계학의의(P＜0.05).유생소D3간예PANC1세포24 h후,음성대조조급25、50、75、100 μmol/L조세포적PTCH mRNA표체량분별위0.117±0.009、0.104 ±0.011、0.069±0.011、0.052±0.009、0.056±0.007;Gli-1 mRNA표체량분별위0.323±0.007、0.312±0.015、0.299±0.015、0.233 ±0.007、0.175 ±0.014,균수농도적증가이하조,차이유통계학의의(P치균＜0.05).75 μmol/L유생소D3간예0、12、24、36、48 h후,PTCH mRNA표체량분별위0.142±0.008、0.127 ±0.009、0.111±0.010、0.115 ±0.003、0.102±0.007;Gli-1 mRNA분별위0.341±0.011、0.317 ±0.017、0.320±0.018、0.226 ±0.011、0.191±0.010,균수시간적연장이하조,차이유통계학의의(P치균＜0.05).결론 유생소D3가이유효억제이선암PANC1세포적증식,촉진세포조망,기궤제가능여조체Hedgehog신호통로유관.
Objective To investigate the role of vitamin D3 in anti-pancreatic cancer.Methods After treatment of different concentrations of vitamin D3 on PANC1 cells (25,50,75,100μmol/L),MTT assay was used to detect the growth inhibition rates of PANC1 cells,the early apoptotic rates of the cell were detected by flow cytometry,PTCH and Gli-1 mRNA expression were detected by RT-PCR method,and cells without treatment were used as control.Results The vitamin D3 inhibited the proliferation of PANC1 cells in a dose-dependent manner,the highest inhibition rate was at 48 hours.After 48 hours,the control group,25,50,75,100 μmol/L vitamin D3 groups' inhibition rates were 0,16.1％,18.8％,31.8％ and 39.4％,the differences among these groups were statistically significance (P ＜ 0.05).After 24 hours,the control group,25,50,75,100μmol/L vitamin D3 groups' early apoptotic rates were (5.89 ±0.57)％,(6.06 ±0.44)％,(16.21 ± 1.62)％,(16.94± 0.91)％ and (20.96 ± 0.98)％,early apoptotic rates were inhibited in a dose-dependent manner,and the differences was statistically significance (P ＜ 0.05).After 24 hours,the control group,25,50,75,100μmol/L vitamin D3 groups' PTCH mRNA expression were 0.117 ± 0.009,0.104 ± 0.011,0.069 ± 0.011,0.052 ± 0.009 and 0.056 ± 0.007,meanwhile the Gli-1 mRNA expressions were 0.323 ± 0.007,0.312 ± 0.015,0.299 ± 0.015,0.233 ± 0.007 and 0.175 ± 0.014,all in a declining trend with the increase of concentration,and the difference was statistically significant (P ＜ 0.05).After 75 μmol/L vitamin D3's intervention in 0,12,24,36 and 48 hours,the expression of PTCH mRNA were 0.142±0.008,0.127± 0.009,0.111± 0.010,0.115± 0.003 and 0.102± 0.007,meanwhile the expression of Gli-1 mRNA were 0.341 ± 0.011,0.317 ± 0.017,0.320 ± 0.018,0.226 ± 0.011 and 0.191 ±0.010,all in a declining trend with time,and the difference was statistically significance (p＜0.05).Conclusions Vitamin D3 can effectively inhibit the proliferation of PANC1 cells and promote its apoptosis,and these effects may be related to blocking of hedgehog signaling pathway.
