Synthesis of [18F]‐labeled adenosine analogues as potential PET imaging agents

The syntheses of adenosine analogues, 2′‐deoxy‐2′‐[¹⁸F]fluoro‐9‐β‐D ‐arabinofuranosyladenine ([¹⁸F]‐FAA) and 3′‐deoxy‐3′‐[¹⁸F]fluoro‐9‐β‐D ‐xylofuranosyladenine ([¹⁸F]‐FXA) are reported. Adenosine ( 1 ) was converted to its methoxytrityl derivatives 2 and 3 as a mixture. After separation, these derivatives were converted to their respective triflates 4 and 5 . Each triflate was reacted with tetrabutylammonium[¹⁸F]fluoride to produce 6b or 7b , which by acidic hydrolysis yielded compounds 8b and 9b . Crude preparations were purified by HPLC to obtain the desired pure products. The radiochemical yields were 10‐18% decay corrected (d. c.) for 8b and 30‐40% (d. c.) for 9b in 4 and 3 runs, respectively. Radiochemical purity was >99% and specific activity was >74 GBq/μmol at the end of synthesis (EOS). The synthesis time was 90‐95 min from the end of bombardment (EOB). Copyright © 2003 John Wiley & Sons, Ltd.     

腺苷A1受体和NMDA受体在海马齿状回突触传递活动中的关系

目的　探讨腺苷A1受体阻断剂对海马齿状回 (DG)突触传递活动的影响及其与NMDA受体的关系。方法采用在体记录麻醉大鼠LTP的电生理学方法 ,观察腺苷A1受体特异性阻断剂 8 环戊 1,3 二丙基黄嘌呤 (DPCPX)与NMDA受体激动剂、阻断剂在海马DG基础突触传递活动和高频刺激诱导的LTP中作用的相关性。结果　DPCPX(6mg·L- 1,5μL ,icv)或NMDA(0 2mg·L- 1,5μL ,icv)不影响大鼠海马DG突触传递活动 ,DPCPX对icvNMDA后高频刺激诱导已形成的LTP维持也无影响 ;预先给予DPCPX后则可显著增强NMDA的海马DG基础突触传递活动和LTP ;AP5(0 5mg·L- 1,5μL)阻断NMDA受体后对LTP的抑制作用不受DPCPX的影响 ,但预先给予DPCPX则可取消AP5 对LTP的抑制作用。结论　DPCPX不影响海马DG突触传递活动 ,但可影响NMDA受体的效应 ,增强NMDA受体在海马DG突触传递活动中的作用     

卷柏化学成分研究卷柏化学成分研究

目的研究中药卷柏(Selaginella tamariscina (Beauv.) Spring)水提物中的化学成分。方法利用Sephadex LH-20及硅胶等色谱技术进行分离纯化,根据理化性质、光谱数据进行结构鉴定。结果得到4个化合物,分别鉴定为1-羟基-2-［2-羟基-3-甲氧基-5-(1-羟基乙基)-苯基］-3-(4-羟基-3,5-二甲氧基苯基)-丙烷-1-O-β-D-葡糖苷(卷柏苷B,I),腺苷(II),鸟苷(III),熊果苷(IV)。结论卷柏苷B为新化合物,腺苷、熊果苷、鸟苷为首次从卷柏属植物中分离得到。     

腺苷A_1受体参与兔脊髓缺血预适应的保护作用

目的　探讨腺苷A1 受体是否参与兔脊髓缺血预适应 (IPC)的保护作用。方法　采用腹主动脉肾下段夹闭法建立兔脊髓缺血模型。动物分为 7组 ,即缺血损伤组 :使脊髓缺血 2 0min ;IPC组 :脊髓预缺血 6min ,再灌注 30min后再次使脊髓缺血 2 0min;8 环戊基 1 ,3 二丙黄嘌呤 (DPCPX ,腺苷A1 受体阻断剂 ) +IPC组及DMSO溶剂 +IPC组 :在IPC前分别ipDPCPX及DMSO ,其余步骤同IPC组 ;DPCPX +缺血损伤组 :在脊髓 2 0min缺血前ipDPCPX ,其余步骤同缺血损伤组 ;预缺血组 :使脊髓缺血 6min;DPCPX +预缺血组 :在脊髓 6min缺血前ipDPCPX ,其余步骤同预缺血组。所有组再灌注48h后 ,进行后肢神经功能评分 ,然后取脊髓进行组织病理学观察。结果　与缺血损伤组相比 ,IPC明显改善脊髓缺血后兔后肢神经功能和减轻脊髓病理学损伤 ;DPCPX完全取消IPC对脊髓缺血的保护作用 ,而DMSO不能取消IPC的保护作用 ;单给DPCPX并不能进一步加重缺血损伤。缺血 6min及DPCPX +缺血 6min均不能引起脊髓缺血损伤。结论　腺苷A1 受体参与兔脊髓IPC的保护作用     

吡啶-2,6(1H,3H)二酮生物碱对ADP、AA、Collagen诱导的兔血小板聚集的影响

目的观察吡啶－２，６（１Ｈ，３Ｈ）二酮生物碱（ＳＨ１）对ＡＤＰ、ＡＡ、Ｃｏｌｌａｇｅｎ诱导的兔血小板聚集的影响。方法用比浊法测定了ＳＨ１体外对兔血小板聚集的影响。结果ＳＨ１对３种诱导剂的最大抑制率分别为６２．１６％、４５．２５％、５３．６７％。大剂量组明显加快ＡＤＰ诱导的兔血小板聚集后的解聚速度。ＳＨ１显著延长Ｃｏｌａｇｅｎ的诱导起聚时间。结论ＳＨ１０．８～４．０ｍｍｏｌＬ－１范围内明显抑制ＡＡ、ＡＤＰ、Ｃｏｌａ－ｇｅｎ诱导的兔血小板聚集。其抑制作用有明显的量效关系。其机制待进一步研究。     

高效液相色谱法测定地黄中腺苷含量

目的:建立地黄中腺苷含量的测定方法,测定不同品种地黄中腺苷的含量。方法:采用高效液相色谱法测定地黄中腺苷含量。以KYWG-C₁₈为固定相,6%乙腈为流动相,检测波长为260nm。结果:腺苷在0.002mg/ml～0.01mg/ml线性良好。回归方程为Y=1.7742×10-4+8.9021×10-7X,r=0.9995。平均回收率为94.1%。RSD=1.86%(n=5)。结论:本法简便、快速、结果可靠。     

实验性脑损伤后脑组织内腺苷、肌苷含量的变化及其意义

研究大鼠急性脑损伤后腺苷含量变化及其生代代谢。方法：采用大鼠液压脑损伤模型,用高效液相色谱法测定大鼠脑损伤前后脑皮质内腺苷和肌苷含量。结果：大鼠脑损伤后１０ｍｉｎ,伤侧大脑皮质内腺苷含量即明显升高,与对伤后３０ｍｉｎ升至最高值,伤后２ｈ腺苷含量恢复正常水平。结论腺苷参与继发性脑损伤后的病理生理过程。     

Marked enhancement of anti-allodynic effect by combined intrathecal administration of the adenosine A1-receptor agonist R-phenylisopropyladenosine and morphine in a rat model of central pain

BACKGROUND: There is often no satisfactory treatment for chronic pain after spinal cord injury. We have previously reported that intrathecal (i.t.) administration of the adenosine A1-receptor agonist R-phenylisopropyl-adenosine (R-PIA) or the opioid morphine has anti-allodynic effects in a model of presumed chronic central pain after photochemically induced spinal cord injury in rats. In the present study, we set out to investigate the possible interaction between i.t. R-PIA and morphine in spinally injured rats. METHODS: Sprague-Dawley rats displaying allodynia-like behaviors to mechanical and cold stimuli after photochemically induced spinal cord injury with minor motor deficits were used. R-PIA and morphine, either alone or in combination, were administered i.t. through an implanted catheter to lumbar spinal cord. RESULTS: Cumulative doses of R-PIA or morphine dose-dependently reduced the mechanical allodynia-like behavior, with a threshold of 1 nmol and 1.5 nmol, respectively. When co-administrated, R-PIA and morphine produced marked suppression of mechanical allodynia at doses of 5 pmol and 7.5 pmol, respectively. The effect of i.t. co-administration of R-PIA and morphine on cold allodynia was comparable to i.t. R-PIA alone. The combination of R-PIA and morphine did not increase adverse effects such as motor deficits in comparison to either drug alone. CONCLUSION: These results demonstrate a supra-additive interaction between the adenosine A1-receptor agonist R-PIA and morphine to reduce mechanical allodynia-like behavior in rats with chronic spinal cord injury. The combination of R-PIA and morphine administered spinally may be superior to R-PIA or morphine alone for treating such pain.     

肺结核患者外周血腺苷脱氨酶活性与淋巴细胞的相关性研究

目的探讨肺结核患者外周血淋巴细胞内腺苷脱氨酶(ADA)活性和全血淋巴细胞绝对值的相关性。方法用全自动生化分析仪及全血细胞计数仪分别测定肺结核患者外周血的ADA活性和淋巴细胞绝对值、比值。结果肺结核活动期组与非活动期组外周血ADA活性均显著高于正常人组(P<0.05),肺结核活动期组与非活动期组患者外周血ADA活性与淋巴细胞绝对值的相关系数分别为0.191和0.154,P>0.05。结论肺结核患者淋巴细胞内ADA活性升高,淋巴细胞绝对值及比值减低,肺结核患者淋巴细胞内ADA活性升高与淋巴细胞绝对值无明显相关。     

吗啡对PC12细胞嘌呤核苷酸代谢相关酶基因表达的影响

目的：研究吗啡对神经细胞模型PC12嘌呤核苷酸补救合成酶与分解代谢关键酶基因表达的影响。方法：采用逆转录聚合酶链反应（RT-PCR）方法检测暴露于吗啡不同时间的PC12细胞次黄嘌呤-鸟嘌呤磷酸核糖转移酶（HGPRT）、腺苷激酶（AK）和腺苷脱氨酶（AD A）mRNA的表达水平。结果：与相应时段对照组相比，PC12细胞暴露于吗啡12及24 h时，HGPRT mRNA水平均明显增高(P<0.05)，作用48 h时HGPRT mRNA水平显著降低(P<0.05)，72 h后HGPRT mRNA水平再次升高(P<0.05)；吗啡处理的PC12细胞于12和24 h时，AK mRNA水平均明显降低(P<0.05)，作用48 h时AK mRNA水平升高(P<0.05)，72 h后AK mRNA水平恢复正常；ADA mRNA水平均表现为轻度降低，12 h差异有显著性(P<0.05)。结论：吗啡影响神经细胞嘌呤核 苷酸代谢，使细胞内腺苷酸及腺苷水平增高，这可能是吗啡依赖和耐受形成的机理之一 。