中华放射医学与防护杂志
中華放射醫學與防護雜誌
중화방사의학여방호잡지
Chinese Journal of Radiological Medicine and Protection
2010年
5期
568-571
,共4页
王明明%司原%陶新全%张伍魁%谢强%谢吉奎
王明明%司原%陶新全%張伍魁%謝彊%謝吉奎
왕명명%사원%도신전%장오괴%사강%사길규
18氟-氟代脱氧葡萄糖%细胞凋亡%Bcl-2蛋白%Bax蛋白
18氟-氟代脫氧葡萄糖%細胞凋亡%Bcl-2蛋白%Bax蛋白
18불-불대탈양포도당%세포조망%Bcl-2단백%Bax단백
18F-FDG%Apoptosis%Bcl-2 protein%Bax protein
目的 研究不同浓度18氟-氟代脱氧葡萄糖(18F-FDG)对Lewis肺癌细胞增殖的影响,探讨其作用机制.方法 以0、0.37、1.85、3.70和7.4(×106 Bq/ml)18F-FDG处理细胞24 h,用倒置显微镜与电子显微镜观察细胞形态学改变,流式细胞术检测细胞凋亡与细胞周期时相分布,3H-TdR掺入法检测细胞DNA合成,比色法检测细胞脂质过氧化水平,免疫组织化学法检测细胞Bcl-2和Bax蛋白的表达.结果 细胞的累积吸收剂量分别为0、0.1l、0.55、1.10与2.20 Gy.受照细胞出现凋亡形态学改变,在0~2.20 Gy剂量范围内,细胞凋亡率由(4.05±0.01)%增大为(25.6±0.28)%(t=188,P<0.01),3H-TdR掺入率从100%下降为(22.0±0.51)%(t=27.6,P<0.05),细胞内丙二醛(MDA)含量由(0.08±0.03)上升到(0.67±0.12)μmol/L(t=11.7,P<0.01).Bcl-2蛋白表达降低,Bax蛋白表达增高,细胞周期发生G2/M期阻滞.结论 18F-FDG能诱导Lewis肺癌细胞凋亡,抑制细胞增殖.
目的 研究不同濃度18氟-氟代脫氧葡萄糖(18F-FDG)對Lewis肺癌細胞增殖的影響,探討其作用機製.方法 以0、0.37、1.85、3.70和7.4(×106 Bq/ml)18F-FDG處理細胞24 h,用倒置顯微鏡與電子顯微鏡觀察細胞形態學改變,流式細胞術檢測細胞凋亡與細胞週期時相分佈,3H-TdR摻入法檢測細胞DNA閤成,比色法檢測細胞脂質過氧化水平,免疫組織化學法檢測細胞Bcl-2和Bax蛋白的錶達.結果 細胞的纍積吸收劑量分彆為0、0.1l、0.55、1.10與2.20 Gy.受照細胞齣現凋亡形態學改變,在0~2.20 Gy劑量範圍內,細胞凋亡率由(4.05±0.01)%增大為(25.6±0.28)%(t=188,P<0.01),3H-TdR摻入率從100%下降為(22.0±0.51)%(t=27.6,P<0.05),細胞內丙二醛(MDA)含量由(0.08±0.03)上升到(0.67±0.12)μmol/L(t=11.7,P<0.01).Bcl-2蛋白錶達降低,Bax蛋白錶達增高,細胞週期髮生G2/M期阻滯.結論 18F-FDG能誘導Lewis肺癌細胞凋亡,抑製細胞增殖.
목적 연구불동농도18불-불대탈양포도당(18F-FDG)대Lewis폐암세포증식적영향,탐토기작용궤제.방법 이0、0.37、1.85、3.70화7.4(×106 Bq/ml)18F-FDG처리세포24 h,용도치현미경여전자현미경관찰세포형태학개변,류식세포술검측세포조망여세포주기시상분포,3H-TdR참입법검측세포DNA합성,비색법검측세포지질과양화수평,면역조직화학법검측세포Bcl-2화Bax단백적표체.결과 세포적루적흡수제량분별위0、0.1l、0.55、1.10여2.20 Gy.수조세포출현조망형태학개변,재0~2.20 Gy제량범위내,세포조망솔유(4.05±0.01)%증대위(25.6±0.28)%(t=188,P<0.01),3H-TdR참입솔종100%하강위(22.0±0.51)%(t=27.6,P<0.05),세포내병이철(MDA)함량유(0.08±0.03)상승도(0.67±0.12)μmol/L(t=11.7,P<0.01).Bcl-2단백표체강저,Bax단백표체증고,세포주기발생G2/M기조체.결론 18F-FDG능유도Lewis폐암세포조망,억제세포증식.
Objective To investigate the influence of 18F-FDG on the proliferation of Lewis lung cancer cell line,and to elucidate its possible mechanism.Methods Morphological changes of cells after culture for 24 h at different concentrations of 0,0.37,1.85,3.70 and 7.4 (×106) Bq/ml of 18F-FDG were observed by using inverted microscopy and electron microscopy.The apoptosis and phase distribution of cell cycle of irradiated cells were analyzed with flow cytometry.DNA synthesis of irradiated cells was assayed by 3H-TdR incorporation.Lipid peroxidation was measured by chromometry and expression of Bcl-2 and Bax protein was measured by immunohistochemical technique.Results Exposed to (0-7.40) × 106Bq/ml of 18F-FDG for 24 h,the cumulative absorbed doses delivered to cells in five groups were 0,0.11,0.55,1.10 and 2.20 Gy,respectively.Irradiated cells showed morphological changes of apoptosis.The apoptosis rate of irradiated cells was increased from (4.05 ± 0.01)% to (25.6 ± 0.28) % (t = 188,P<0.01).3H-TdR incorporation rate was decreased from 100% to(22.0 ± 0.51)% (t =27.6,P <0.05).The levels of M DA in cells were augmented from (0.08 ± 0.03) to (0.67 ± 0.12) μmol/L (t =11.7,P < 0.01).Cell cycle arrest was found in G2/M phase with the increasing doses from 0 to 2.20 Gy.The expression of Bcl-2 protein was decreased while that of Bax protein increased.Conclusions 18F-FDG could induce the apoptosis of cells and inhibit the proliferation of cells.