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作 者:谢良骏[1] 秦露平[1] 李建芳[1] 曾凤伟[1] 袁海娟[1] 林主戈 张峰[1] 程木华[1]
机构地区:[1]中山大学附属第三医院核医学科,广州510630
出 处:《广东医学》2015年第3期333-335,共3页Guangdong Medical Journal
基 金:广东省自然科学基金资助项目(编号:S2012010009273)
摘 要:目的探讨地塞米松对肝癌细胞聚集18F-FDG能力的影响。方法根据地塞米松浓度将肝癌细胞HepG2和正常肝细胞L02分为0、10-8、10-7、10-6、10-5、10-4mol/L浓度处理组,每组均各设平行孔,对各组HepG2细胞和L02细胞预处理2、4、6、8、12、24 h,然后向各组加入1μCi18F-FDG孵育1 h,应用计数仪检测各组细胞的放射性计数。结果对HepG2细胞,当地塞米松浓度为10-8、10-7mol/L时,放射性计数减小(P<0.05),当地塞米松浓度为10-5、10-4mol/L时,放射性计数增高(P<0.05)。对L02细胞,当地塞米松浓度为10-8、10-7、10-6mol/L时,放射性计数减小(P<0.05),当地塞米松浓度为10-4mol/L时,放射性计数增高(P<0.05)。每组HepG2细胞18F-FDG放射性计数均高于L02细胞(P<0.05),且经地塞米松处理后,两种细胞放射性计数差值增大(P<0.05)。结论地塞米松对肝脏细胞聚集18F-FDG存在双向调节作用,适量浓度可以扩大肝癌细胞与正常肝细胞摄取18F-FDG的差异。Objective To enhance the 18 F-FDG uptake capacity of hepatic carcinoma cells .Methods Hepatic carcinoma cell HepG2 and normal hepatic cell L02 were incubated for 2 h, 4 h, 6 h, 8 h, 12 h and 24 h with the dexam-ethasone of 10-8 mol/L,10-7 mol/L,10-6 mol/L,10-5 mol/L or 10-4 mol/L.The control group was treated without dexa -methasone.After that, 1 μCi 18 F -FDG was added for incubation into each group for 1 h, and the radioactivity counts were assessed subsequently.Results Dexamethasone significantly inhibited uptake capacity of the 18 F -FDG in HepG2 with the concentrations of 10-8 mol /L and 10-7 mol /L; promoted it with concentrations of 10-5 mol/L and 10-4 mol/L;and had no effect on it with the concentration of 10-6 mol/L (P &lt;0.05).Meanwhile, Dexamethasone significantly inhibi -ted uptake capacity of the 18 F -FDG in L02 with the concentrations of 10-8 mol/L, 10-7 mol/L and 10-6 mol/L; promo-ted it with concentrations of 10-4 mol /L; and had no effect on it with the concentration of 10-5 mol/L (P &lt;0.05).The 18 F -FDG uptake capacity of HepG2 was significantly higher than L02, and the difference was significantly enlarged by pre -treatment by dexamethasone (P &lt;0.05).Conclusion Dexamethasone has biphasic effect on the 18 F -FDG uptake capacity of hepatocytes.The appropriate concentration of dexamethasone can enlarge the 18 F -FDG uptake difference be-tween HepG2 and L02.
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