医药导报
醫藥導報
의약도보
HERALD OF MEDICINE
2014年
10期
1321-1325
,共5页
赵宁%黄永吉%马广斌%严冬雪
趙寧%黃永吉%馬廣斌%嚴鼕雪
조저%황영길%마엄빈%엄동설
鞣花酸%骨髓瘤%SP2/0细胞%增殖%凋亡
鞣花痠%骨髓瘤%SP2/0細胞%增殖%凋亡
유화산%골수류%SP2/0세포%증식%조망
Ellagic acid%Multiple myeloma%SP2/0 cell lines%Proliferation%Apoptosis
目的:探讨五倍子提取物鞣花酸抗骨髓瘤的生物学活性及相关机制。方法20,40和60μg·mL-1鞣花酸体外孵育骨髓瘤 SP2/0细胞株,采用细胞形态学、细胞增殖实验和流式细胞仪检测鞣花酸对 SP2/0细胞株增殖、凋亡和细胞周期的影响,通过 Western blotting 技术检测肿瘤细胞增殖与凋亡相关基因 COX-2的表达。结果20,40,60μg·mL-1鞣花酸孵育骨髓瘤 SP2/0细胞株48 h 后,细胞周期阻滞于 G1期,G1期细胞百分率分别为(55.21±3.01)%,(64.48±0.43)%,(75.10±2.46)%,与对照组(34.04±1.74)%比较,差异有统计学意义( P <0.01)。20,40和60μg·mL-1鞣花酸细胞抑制率分别为(21.18±5.92)%,(44.58±3.43)%和(70.15±2.90)%,与对照组比较,差异有统计学意义(P<0.01)。细胞早期凋亡率分别为(9.60±0.56)%,(19.30±1.51)%和(35.10±5.26)%,与对照组(3.23±0.85)%比较,差异有统计学意义(P<0.01),随药物浓度的增加 COX-2的表达逐渐下降。结论鞣花酸能够抑制骨髓瘤SP2/0细胞增殖,促进其凋亡。
目的:探討五倍子提取物鞣花痠抗骨髓瘤的生物學活性及相關機製。方法20,40和60μg·mL-1鞣花痠體外孵育骨髓瘤 SP2/0細胞株,採用細胞形態學、細胞增殖實驗和流式細胞儀檢測鞣花痠對 SP2/0細胞株增殖、凋亡和細胞週期的影響,通過 Western blotting 技術檢測腫瘤細胞增殖與凋亡相關基因 COX-2的錶達。結果20,40,60μg·mL-1鞣花痠孵育骨髓瘤 SP2/0細胞株48 h 後,細胞週期阻滯于 G1期,G1期細胞百分率分彆為(55.21±3.01)%,(64.48±0.43)%,(75.10±2.46)%,與對照組(34.04±1.74)%比較,差異有統計學意義( P <0.01)。20,40和60μg·mL-1鞣花痠細胞抑製率分彆為(21.18±5.92)%,(44.58±3.43)%和(70.15±2.90)%,與對照組比較,差異有統計學意義(P<0.01)。細胞早期凋亡率分彆為(9.60±0.56)%,(19.30±1.51)%和(35.10±5.26)%,與對照組(3.23±0.85)%比較,差異有統計學意義(P<0.01),隨藥物濃度的增加 COX-2的錶達逐漸下降。結論鞣花痠能夠抑製骨髓瘤SP2/0細胞增殖,促進其凋亡。
목적:탐토오배자제취물유화산항골수류적생물학활성급상관궤제。방법20,40화60μg·mL-1유화산체외부육골수류 SP2/0세포주,채용세포형태학、세포증식실험화류식세포의검측유화산대 SP2/0세포주증식、조망화세포주기적영향,통과 Western blotting 기술검측종류세포증식여조망상관기인 COX-2적표체。결과20,40,60μg·mL-1유화산부육골수류 SP2/0세포주48 h 후,세포주기조체우 G1기,G1기세포백분솔분별위(55.21±3.01)%,(64.48±0.43)%,(75.10±2.46)%,여대조조(34.04±1.74)%비교,차이유통계학의의( P <0.01)。20,40화60μg·mL-1유화산세포억제솔분별위(21.18±5.92)%,(44.58±3.43)%화(70.15±2.90)%,여대조조비교,차이유통계학의의(P<0.01)。세포조기조망솔분별위(9.60±0.56)%,(19.30±1.51)%화(35.10±5.26)%,여대조조(3.23±0.85)%비교,차이유통계학의의(P<0.01),수약물농도적증가 COX-2적표체축점하강。결론유화산능구억제골수류SP2/0세포증식,촉진기조망。
Objective To investigate the effect of ellagic acid extracted from gallnut on multiple myeloma SP2 / 0 cell line and related mechanisms. Methods Multiple myeloma SP2 / 0 cell line was treated for 48 h with different concentrations of ellagic acid in vitro. Cell morphology,proliferation,apoptosis and cell cycle were analyzed with microscope,MTT experiment and flow cytometry,respectively. Tumor cell proliferation and apoptosis-related gene expression of COX-2 were detected by Western blotting. Results Cell cycle was arrested at the G1 phase 48 h after treatment with ellagic acid, the cell in G1 were (55. 21±3. 01)% , (64. 48 ± 0. 43)% , (75. 10 ± 2. 46)% , respectively, with significant difference as compared with control group [(34. 04±1. 74)% ,P<0. 01]. Cell suppression rate (21. 18±5. 92)% ,(44. 58±3. 43)% and (70. 15±2. 90)% ,respectively, in 20,40 and 60 μg·mL-1 ellagic acid treatment groups. Compared with the control group,the differences were significant (P<0. 01). Cell apoptosis rate was (9. 60 ± 0. 56)% , (19. 30 ± 1. 51)% and (35. 10 ± 5. 26)% , respectively, in 20,40 and 60 μg·mL-1 ellagic acid treatment groups,with significant differences as compared with the control group[(3. 23±0. 85)% ,P<0. 01]. With the increase of drug concentration,COX-2 expression was decreased. Conclusion Ellagic acid can inhibit myeloma SP2 / 0 cell proliferation and promote apoptosis.