中华生物医学工程杂志
中華生物醫學工程雜誌
중화생물의학공정잡지
CHINESE JOURNAL OF BIOMEDICAL ENGINEERING
2012年
1期
41-44
,共4页
邓怀福%唐刚华%陈萍%王红亮%孟悛非
鄧懷福%唐剛華%陳萍%王紅亮%孟悛非
산부복%당강화%진평%왕홍량%맹전비
S-11C-甲基-L-半胱氨酸%氨基酸转运系统,中性%正电子发射断层显像术%肝肿瘤,实验性%细胞摄取
S-11C-甲基-L-半胱氨痠%氨基痠轉運繫統,中性%正電子髮射斷層顯像術%肝腫瘤,實驗性%細胞攝取
S-11C-갑기-L-반광안산%안기산전운계통,중성%정전자발사단층현상술%간종류,실험성%세포섭취
S - 11C - methyl - L - cysteine%Amino acid transport systems,neutral%Positron -emission tomography%Liver neoplasms,experimental%Cell uptake
目的 探讨肿瘤细胞摄取S-11C-甲基-L-半胱氨酸(11C-MCYS)的机制.方法 将Hepa1-6肝癌细胞分为Na+依赖组(NaCl组)及非Na+依赖组(氯化胆碱组)进行氨基酸转运实验.每组又分为对照组、L-氨基酸转运载体抑制剂2-氨基二环-2,2,1-庚烷-2-羧酸(BCH)组、转运系统A和ASC的抑制剂α-甲基-氨基异丁酸(MeAIB)组、MeAIB+丝氨酸组,分别加入11C-MCYS(400μ1 0.925 MBq/ml)、11C-MCYS(200μl 1.85 MBq/ml)+阻滞剂BCH(200μl 15 mmol/L)、11C-MCYS(200μl 1.85 MBq/ml)+阻滞剂MeAIB(200μl 15 mmol/L)以及11C-MCYS (200μl 1.85 MBq/ml)+阻滞剂MeAIB+丝氨酸(200μl15 mmol/L).作用4 min后终止培养应用γ计数仪测量细胞放射性活度.将Hepal-6肝癌细胞分为5组,各组均加入200 μl11C-MCYS( 1.85 MBq/ml)后分别加入50、100、200、300、350μmol/L浓度不等的MCYS进行竞争抑制实验.培养4 min后终止培养应用γ计数仪测量细胞放射性活度.结果 无论是否有Na+存在,对照组、BCH组、MeAlB及MeAIB+丝氨酸组对11C-MCYS摄取的差异均无统计学意义(均P＞0.05).MeAIB组和MeAIB+丝氨酸组中的NaC1组细胞放射性活性与氯化胆碱组相比差异均无统计学意义(18 958.18±97.32比20 582.27±196.32,18 385.24±122.96比21 620.54±131.41,均P＞0.05),两者均不能抑制Na+非依赖性氨基酸转运载体的转运.而BCH组中的NaC1组细胞放射性活性高于氯化胆碱组(2587.21±30.25比2340.61±21.09,P＜0.05),可见BCH能明显抑制Na+非依赖性氨基酸转运体对11C-MCYS的转运.不同浓度MCYS(50 ～ 350 μmol/L)作用下肿瘤细胞对11C-MCYS摄取差异无统计学意义(均P＞0.05).结论 肿瘤细胞摄取11C-MCYS是通过非Na+依赖的L-氨基酸转运系统进行转运的,极少涉及氨基酸转运系统A和ASC.
目的 探討腫瘤細胞攝取S-11C-甲基-L-半胱氨痠(11C-MCYS)的機製.方法 將Hepa1-6肝癌細胞分為Na+依賴組(NaCl組)及非Na+依賴組(氯化膽堿組)進行氨基痠轉運實驗.每組又分為對照組、L-氨基痠轉運載體抑製劑2-氨基二環-2,2,1-庚烷-2-羧痠(BCH)組、轉運繫統A和ASC的抑製劑α-甲基-氨基異丁痠(MeAIB)組、MeAIB+絲氨痠組,分彆加入11C-MCYS(400μ1 0.925 MBq/ml)、11C-MCYS(200μl 1.85 MBq/ml)+阻滯劑BCH(200μl 15 mmol/L)、11C-MCYS(200μl 1.85 MBq/ml)+阻滯劑MeAIB(200μl 15 mmol/L)以及11C-MCYS (200μl 1.85 MBq/ml)+阻滯劑MeAIB+絲氨痠(200μl15 mmol/L).作用4 min後終止培養應用γ計數儀測量細胞放射性活度.將Hepal-6肝癌細胞分為5組,各組均加入200 μl11C-MCYS( 1.85 MBq/ml)後分彆加入50、100、200、300、350μmol/L濃度不等的MCYS進行競爭抑製實驗.培養4 min後終止培養應用γ計數儀測量細胞放射性活度.結果 無論是否有Na+存在,對照組、BCH組、MeAlB及MeAIB+絲氨痠組對11C-MCYS攝取的差異均無統計學意義(均P＞0.05).MeAIB組和MeAIB+絲氨痠組中的NaC1組細胞放射性活性與氯化膽堿組相比差異均無統計學意義(18 958.18±97.32比20 582.27±196.32,18 385.24±122.96比21 620.54±131.41,均P＞0.05),兩者均不能抑製Na+非依賴性氨基痠轉運載體的轉運.而BCH組中的NaC1組細胞放射性活性高于氯化膽堿組(2587.21±30.25比2340.61±21.09,P＜0.05),可見BCH能明顯抑製Na+非依賴性氨基痠轉運體對11C-MCYS的轉運.不同濃度MCYS(50 ～ 350 μmol/L)作用下腫瘤細胞對11C-MCYS攝取差異無統計學意義(均P＞0.05).結論 腫瘤細胞攝取11C-MCYS是通過非Na+依賴的L-氨基痠轉運繫統進行轉運的,極少涉及氨基痠轉運繫統A和ASC.
목적 탐토종류세포섭취S-11C-갑기-L-반광안산(11C-MCYS)적궤제.방법 장Hepa1-6간암세포분위Na+의뢰조(NaCl조)급비Na+의뢰조(록화담감조)진행안기산전운실험.매조우분위대조조、L-안기산전운재체억제제2-안기이배-2,2,1-경완-2-최산(BCH)조、전운계통A화ASC적억제제α-갑기-안기이정산(MeAIB)조、MeAIB+사안산조,분별가입11C-MCYS(400μ1 0.925 MBq/ml)、11C-MCYS(200μl 1.85 MBq/ml)+조체제BCH(200μl 15 mmol/L)、11C-MCYS(200μl 1.85 MBq/ml)+조체제MeAIB(200μl 15 mmol/L)이급11C-MCYS (200μl 1.85 MBq/ml)+조체제MeAIB+사안산(200μl15 mmol/L).작용4 min후종지배양응용γ계수의측량세포방사성활도.장Hepal-6간암세포분위5조,각조균가입200 μl11C-MCYS( 1.85 MBq/ml)후분별가입50、100、200、300、350μmol/L농도불등적MCYS진행경쟁억제실험.배양4 min후종지배양응용γ계수의측량세포방사성활도.결과 무론시부유Na+존재,대조조、BCH조、MeAlB급MeAIB+사안산조대11C-MCYS섭취적차이균무통계학의의(균P＞0.05).MeAIB조화MeAIB+사안산조중적NaC1조세포방사성활성여록화담감조상비차이균무통계학의의(18 958.18±97.32비20 582.27±196.32,18 385.24±122.96비21 620.54±131.41,균P＞0.05),량자균불능억제Na+비의뢰성안기산전운재체적전운.이BCH조중적NaC1조세포방사성활성고우록화담감조(2587.21±30.25비2340.61±21.09,P＜0.05),가견BCH능명현억제Na+비의뢰성안기산전운체대11C-MCYS적전운.불동농도MCYS(50 ～ 350 μmol/L)작용하종류세포대11C-MCYS섭취차이무통계학의의(균P＞0.05).결론 종류세포섭취11C-MCYS시통과비Na+의뢰적L-안기산전운계통진행전운적,겁소섭급안기산전운계통A화ASC.
Objective To investigate the mechanism in uptake of S-11C-methyl-L-cysteine(11C-MCYS) by tumor cells.Methods Hepal-6 cells were divided into Na+ dependent (NaC1 group) and nonNa+ dependent (choline chloride group) groups for amino acids transport experiment.The two groups were then divided into control group,2' - aminobicyclo (2,2,1 ) - heptane-2' - carboxylic acid (BCH,L- amino acid transporter inhibitor),N-methylamino-isobutyric acid (MeAIB,transport system inhibitor of A and ASC) and MeAIB+serine groups.All the groups were added with 11C-MCYS (400 μl 0.925 MBq/ml),11C-MCYS(200μ1 1.85 MBq/ml)+ BCH(200 μ1 15 mmol/L),11C-MCYS(200 μl 1.85 MBq/ml)+ MeAIB(200μl 15 mmol/L),11C-MCYS(200 μ1 1.85 MBq/ml)+ MeAIB+serine(200 μ1 15 mmol/L) respectively.After 4min,the incubation was discontinued,and the cell radioactivity was measured with γ counter.Thereafter,Hepa 1-6 cells were classified into five groups which were added with 200 μl 11C-MCYS( 1.85 MBq/ml)and then different concentrations of MCYS (50,100,200,300,350 μmol/L) for a competitive inhibition experiment.γcounter was used to measure the radioactivity at 4 mins after incubation.Results There were no significant differences in uptake of 11C- MCYS by control,BCH,MeAIB and MeAIB+serine groups with or without the presence of Na + (P＞0.05).In MeAIB and MeAIB + serine groups,the NaC1 and choline chloride sub- groups showed no significant differences in radioactivity (18 958.18±97.32 vs 20 582.27±196.32,18 385.24± 122.96 vs 21 620.54± 131.41,both P＞0.05)and could not inhibit the transportation of non-Na+ dependent amino acid carrier.However in BCH group,the radioactivity in NaC1 group was higher than that in choline chloride group (2587.21 ± 30.25 vs 2340.61 ± 21.09,P＜0.05).Thus,BCH could significantly inhibit the transportation of 11C-MCYS by non-Na+ dependent amino acid carrier.No significant differences were found in uptake of 11C-MCYS by tumor cells under different concentrations of MCYS (50 ～350 μmol/L) (all P＞0.05).Conclusion The uptake of 11C-MCYS is the result of transportation through nonNa+ dependent L-amino acid transport system,with minimal involvement of amino acid transport system A and ASC.
