中华预防医学杂志
中華預防醫學雜誌
중화예방의학잡지
CHINESE JOURNAL OF
2012年
3期
233-236
,共4页
曾强%崔玉山%张磊%符刚%侯常春%赵亮%王爱国%刘洪亮
曾彊%崔玉山%張磊%符剛%侯常春%趙亮%王愛國%劉洪亮
증강%최옥산%장뢰%부강%후상춘%조량%왕애국%류홍량
氟化物%甲状腺%细胞凋亡%氧化性应激%细胞周期
氟化物%甲狀腺%細胞凋亡%氧化性應激%細胞週期
불화물%갑상선%세포조망%양화성응격%세포주기
Fluorides%Thyroid gland%Apoptosis%Oxidative stress%Cell cycle
目的 探讨氟对人正常甲状腺细胞Nthy-ori 3-1的毒性作用及机制.方法 分别用0(对照)、0.1、1.0、3.0 mmol/L的NaF作用于体外培养的Nthy-ori 3-1细胞24h后,采用噻唑蓝染色法、乳酸脱氢酶(LDH)比色法检测存活率和LDH漏出率,采用流式细胞术检测活性氧(ROS)水平、细胞周期构成比及凋亡率.结果 以对照组细胞存活率为100%,1.0、3.0 mmol/L NaF组细胞存活率分别为(76.64±9.13)%、(64.04±6.32)%,与对照组存活率的差异有统计学意义(P值均<0.01).3.0 mmol/L NaF组LDH漏出率及ROS水平分别为(48.66±7.15)%,(29 993.50±1786.86),较对照组[分别为(35.24±3.02)%,(13 021.33±1067.55)]升高(P值均<0.01).1.0 mmol/L NaF组细胞G0/G1期、S期细胞百分比分别为(40.76±5.65)%、(54.05±4.59)%,与对照组[分别为(60.09±1.76)%、(32.59±2.43)%]相比,差异有统计学意义(P值均<0.01).3.0 mmol/L NaF组细胞凋亡率为(20.09±3.22)%,高于对照组[(9.64±3.44)%],P<0.01.结论 试验浓度的氟能降低甲状腺细胞存活率,增加LDH漏出率和ROS产生,并使细胞发生S期阻滞及诱导细胞凋亡.
目的 探討氟對人正常甲狀腺細胞Nthy-ori 3-1的毒性作用及機製.方法 分彆用0(對照)、0.1、1.0、3.0 mmol/L的NaF作用于體外培養的Nthy-ori 3-1細胞24h後,採用噻唑藍染色法、乳痠脫氫酶(LDH)比色法檢測存活率和LDH漏齣率,採用流式細胞術檢測活性氧(ROS)水平、細胞週期構成比及凋亡率.結果 以對照組細胞存活率為100%,1.0、3.0 mmol/L NaF組細胞存活率分彆為(76.64±9.13)%、(64.04±6.32)%,與對照組存活率的差異有統計學意義(P值均<0.01).3.0 mmol/L NaF組LDH漏齣率及ROS水平分彆為(48.66±7.15)%,(29 993.50±1786.86),較對照組[分彆為(35.24±3.02)%,(13 021.33±1067.55)]升高(P值均<0.01).1.0 mmol/L NaF組細胞G0/G1期、S期細胞百分比分彆為(40.76±5.65)%、(54.05±4.59)%,與對照組[分彆為(60.09±1.76)%、(32.59±2.43)%]相比,差異有統計學意義(P值均<0.01).3.0 mmol/L NaF組細胞凋亡率為(20.09±3.22)%,高于對照組[(9.64±3.44)%],P<0.01.結論 試驗濃度的氟能降低甲狀腺細胞存活率,增加LDH漏齣率和ROS產生,併使細胞髮生S期阻滯及誘導細胞凋亡.
목적 탐토불대인정상갑상선세포Nthy-ori 3-1적독성작용급궤제.방법 분별용0(대조)、0.1、1.0、3.0 mmol/L적NaF작용우체외배양적Nthy-ori 3-1세포24h후,채용새서람염색법、유산탈경매(LDH)비색법검측존활솔화LDH루출솔,채용류식세포술검측활성양(ROS)수평、세포주기구성비급조망솔.결과 이대조조세포존활솔위100%,1.0、3.0 mmol/L NaF조세포존활솔분별위(76.64±9.13)%、(64.04±6.32)%,여대조조존활솔적차이유통계학의의(P치균<0.01).3.0 mmol/L NaF조LDH루출솔급ROS수평분별위(48.66±7.15)%,(29 993.50±1786.86),교대조조[분별위(35.24±3.02)%,(13 021.33±1067.55)]승고(P치균<0.01).1.0 mmol/L NaF조세포G0/G1기、S기세포백분비분별위(40.76±5.65)%、(54.05±4.59)%,여대조조[분별위(60.09±1.76)%、(32.59±2.43)%]상비,차이유통계학의의(P치균<0.01).3.0 mmol/L NaF조세포조망솔위(20.09±3.22)%,고우대조조[(9.64±3.44)%],P<0.01.결론 시험농도적불능강저갑상선세포존활솔,증가LDH루출솔화ROS산생,병사세포발생S기조체급유도세포조망.
Objective To explore the toxic effect of fluoride on the human thyroid cells ( Nthy-ori 3-1 ) and its mechanism.Methods Nthy-ori 3-1 cells were exposed to 0.0,0.1,1.0,3.0 mmol/L of sodium fluoride (NaF) in vitro.After 24 hours incubation,3 (4,5-Dimethylthiazol-z-y1 )-3,5-diphenyltetrazolium bromide(MTT) assay and lactate dehydrogenase (LDH) assay were used to measure cell viability and the LDH leakage rate.Reactive oxygen species (ROS) level,constituent ratio of the cell cycle,and apoptosis rate were measured by flow cytometry.Results Comparing to viability of control group ( set as 100.00% ),the cell viability of the 1.0,3.0 mmol/L fluoride-treated groups ( 76.64 ± 9.13 ) %,(64.04 ±6.32)% were significantly decreased (all P values <0.01 ).LDH leakage rate and ROS level of the 3.0 mmol/L fluoride-treated group ( (48.66+7.15)%,(29 993.50 ± 1786.86) FI) were significantly increased ( all P values < 0.01 ) compared to control group ( ( 35.24 ± 3.02 ) %,( 13 021.33 ± 1067.55 )FI).The G0/G1 phase cells of the 1.0 mmol/L fluoride-treated group ( (40.76 ±5.65)% ) were lower than control group (60.09 ± 1.76)% (P < 0.01 ),yet the percentage of cells in S phase (( 54.05 ± 4.59 )% )were higher than the control group ( 32.59 ± 2.43 ) % ( P < 0.0l ).Comparing to control group ( ( 9.64 ±3.44) % ),the precentage of apoptosis cells increased in the 3.0 mmol/L fluoride-treated group ( (20.09 ±3.22)%) (P<0.01).Conclusion To Nthy-ori 3-1 cells,fluoride under experimental concentrations decreases cell viability,improve the LDH leakage rate,and ROS leveL It blocks the cells in S phase and induce cell apoptosis.