人参茎叶皂甙对正常和利血平化小鼠心肌cAMP和cGMP含量的影响

口服人参茎叶皂甙25mg/kg,连续服用7天组小鼠心肌 cAMP 含量显著升高(p<0.01),而对 cGMP 含量无明显影响;50mg/kg GSL 对 cAMP,cGMP 含量均无明显影响。对利血平化小鼠,50mg/kg 能明显提高小鼠心肌中 cAMP 的含量(p<0.01),对 cGMP 含量影响不明显。cAMP/cGMP 比值提示,25mg/kg 和50mg/kg GSL 对 cAMP/cGMP 比值均增高;对利血平化小鼠心肌 cAMP/cGMP 比值无明显变化。     

温度通过cAMP及cGMP对人淋巴细胞E受体的影响

作者用放射免疫测定及E玫瑰花环测定法检测了不同温度,不同保存时间对淋巴细胞E受体及细胞内cAMP相cGMP的影响,结果表明,随着温度的降低及保存时间的延长,E玫瑰花环的抑制率逐渐增加(P<0.05及0.01)。淋巴细胞内的cAMP含量升高,cGMP含量稍下降,cAMP/cGMP比值增大(P<0.05及0.01)。并对温度、淋巴细胞E受体及环核苷酸三者之间关系进行探讨。     

支气管哮喘的抗炎症疗法

<正> 支气管哮喘是一种较常见的疾病,发病率约占人口的2％,儿童与成年人都可发病。早期治疗支气管哮喘,可选用拟肾上腺素类药物兴奋支气管平滑肌细胞β受体,提高细胞内的cAMP含量;或选用含黄嘌呤基团的茶碱类药物抑制磷酸二酯酶活性,阻止cAMP转变为5′AMP,以保持细胞内的cAMP含量;或选用阿托品等M受体阻断剂减少细胞内cGMP,以提高cAMP/cGMP比值。但是这些缓解剂只能暂时缓解哮喘症状,难以达到治愈目的。     

慢性支气管炎局部神经功能紊乱对肺泡巨噬细胞的影响

目的 探讨肾上腺素神经和胆碱能神经在慢性支气管炎中的作用及作用机制.方法 分别检测慢性支气管炎（慢支）组、慢性支气管炎合并肺气肿组患者和正常对照组外周血、支气管肺灌洗液（BALF）中胆碱脂酶（ChE）和去甲肾上腺素（NE）的含量,支气管肺泡灌洗液肺泡巨噬细胞内环磷酸腺苷（cAMP）及环磷酸鸟苷（cGMP）含量.结果 慢支组与正常组BALF中ChE无显著差异,而NE升高;在慢支合并肺气肿组患者BALF中ChE较正常组增高,而NE较正常对照组少;慢支组BALF AM内cAMP/cGMP比值正常, 而慢支合并肺气肿组AM内cAMP/cGMP较正常对照组明显降低,β2-受体激动剂（舒喘灵）作用于AM后,慢支组cAMP/cGMP比值上调,而慢支肺气肿组AM内cAMP/cGMP比值无明显变化.结论 肾上腺素神经、胆碱能神经及肾上腺素受体参与了慢性支气管炎的发生发展过程,在不同的疾病阶段其作用不同.     

龙虎黄芪汤对乙肝患者的cAMP、cGMP、LPO、SOD变化的影响

目的研究龙虎黄芪汤对乙肝患者cAMP、cGMP、LPO、SOD变化的影响。方法采用放射免疫比色法分析。结果服用龙虎黄芪汤后cAMP、SOD含量升高,cAMP／cGMP比值增加,LPO减少。     

硒化壳聚糖和亚硒酸钠抗K562细胞的实验研究

应用MTT比色分析法比较研究有机硒化物-硒化壳聚糖和无机硒化物亚硒酸钠对白血病K562细胞的作用。结果表明：两种硒在体外实验浓度范围内均对K562细胞的增殖具有显著的抑制作用，并有剂量反应关系：硒化壳聚糖的抗白血病效应明显高于含同样硒量的亚硒酸钠，约为其3倍，有机硒比无机硒具有更高的抗白血病活性。     

聚酯型儿茶素对HL-60细胞的诱导分化作用及其机制研究

目的　研究聚酯型儿茶素对人急性早幼粒白血病HL 6 0细胞的分化作用并探讨其作用机制。方法　应用电镜、NBT还原试验、同位素掺入试验、细胞内cAMP/cGMP浓度测定、原位杂交和免疫细胞化学等方法研究细胞分化及机制。结果　聚酯型儿茶素作用于HL 6 0细胞后 ,扫描电镜和透射电镜观察显示分化细胞的特征 ;NBT还原能力明显增强 ;[3H] TdR ,[3H] Leu掺入试验证明聚酯型儿茶素可明显抑制细胞DNA和蛋白质合成 ;聚酯型儿茶素作用后 ,细胞内cAMP浓度及cAMP/cGMP比值明显增加 ,HL 6 0细胞的c myc基因mRNA和蛋白产物的表达均明显降低 ,而c fos基因mRNA和蛋白产物的表达均明显升高。结论　聚酯型儿茶素可诱导HL 6 0细胞向成熟细胞分化 ,其分化作用可能与其升高细胞内cAMP/cGMP比值和抑制c myc基因表达、增强c fos基因表达有关。本研究为聚酯型儿茶素在肿瘤防治领域的开发应用提供了充分的理论依据     

钙离子一氧化氮在硒化壳聚糖诱导的皮肤成纤维细胞增殖中的作用

目的观察硒化壳聚糖对体外培养人皮肤成纤维细胞增殖周期及细胞内一氧化氮(NO)水平及钙离子含量的影响。方法皮肤成纤维细胞培养液加入不同浓度的硒化壳聚糖(25、50、100、200、400 mg/L),应用噻唑蓝(MTT)法检测细胞增殖,改良Griess法检测NO,Huo-3AM钙荧光指标剂测定细胞内钙离子浓度,流式细胞仪检测细胞周期。结果与对照组比较,50~400 mg/L硒化壳聚糖作用48 h后,细胞对MTT的吸收明显升高(P<0.05);各浓度硒化壳聚糖组细胞NO水平(72±9)μmol/L~(44±10)μmol/L与对照组(107±9)μmol/L比较均呈不同程度下降,呈剂量依赖性(P<0.01);200、400 mg/L硒化壳聚糖组细胞内钙离子浓度(179±32)mmol/L、(179±14)mmol/L与对照组(147±10)mmol/L比较显著升高(P<0.05);流式细胞分析显示,G0~G1期细胞所占百分率显著性减少,G2~M期和S期细胞所占百分率显著性增加(P<0.01)。结论硒化壳聚糖可通过调节细胞内钙离子含量和NO水平来促进皮肤成纤维细胞增殖。     

抗胆碱药对大鼠血浆环核苷酸含量影响

阿托品4、6、10mg/kg ip可显著地降低大鼠血浆cGMP含量(P<0.05);东莨菪碱、B-7601分别需要10.15mg/kg ip。三药对血浆cAMP含量的影响无统计学意义。唯阿托品6.10mg/kg可提高cAMP/cGMP的比值(P<0.05)。结果提示:三药对大鼠血浆cGMP含量的影响,阿托品>东莨菪碱>B-7601。     

棱曼中毒后家兔脑内环核苷酸和钙调素水平的变化

用放射免疫测定法测定家兔梭曼中毒后小脑cAMP,cGMP含量,发现随梭曼剂量的增加,cAMP、cGMP含量明显升高,而cAMP/cCMP值明显降低。其中当梭曼剂量为25μg/kg时,小脑,桥-延脑cAMP,cGMP含量在中毒30min时最高,cAMP/cGMP值最低,随后开始恢复,在中毒120min时接近对照水平。用PDE法测定家兔大脑皮层的钙调素(CaM)含量(有活性的CaM含量),发现中毒15min时,CaM含量已明显降低,中毒30min时未见恢复。值得提出的是,动物中毒症状的轻重变化过程与cAMP,cGMP含量及cAMP/cGMP值的升降变化过程相吻合。结果提示,梭曼可能通过影响中枢cAMP/cGMP值发挥毒性作用。     

硒化壳聚糖对NB_4细胞的作用及其与NF-κB信号分子的关系

目的:研究硒化壳聚糖对人急性早幼粒细胞性白血病NB4细胞抗氧化指标的影响及其与核因子κB(NF-κB)信号分子的关系。方法:取NB4细胞加入不同浓度的硒化壳聚糖(50、100、200mg·L-1)作用24h后取上清检测谷胱甘肽过氧化物酶(GSH-px)、超氧化物歧化酶(SOD)、丙二醛(MDA)、NF-κB蛋白含量或活性,并设培养液为对照组。结果:与对照组比较,硒化壳聚糖各浓度组GSH-px活性明显升高(P<0.01),SOD活性和MDA含量明显降低(P<0.01或P<0.05),NF-κB蛋白含量明显降低(P<0.01),并呈量效关系。结论:硒化壳聚糖可通过减少进入细胞核内NF-κB蛋白含量的方式下调其下游基因表达,以及增强细胞抗氧化能力的方式抑制NB4细胞增殖,诱导细胞凋亡。     

硒化壳聚糖对HL60细胞的诱导分化作用

目的:研究硒化壳聚糖对人早幼粒细胞性白血病HL60细胞分化的影响,并探讨该影响与细胞c-myc和c-fos蛋白表达的关系。方法:取HL60细胞分为5组,分别为25、50、100mg·L-1硒化壳聚糖组、空白对照组(培养液)和阳性对照组(二甲基亚砜)。各组经相应试药作用后,采用硝基蓝四氮唑(NBT)还原法检测HL60细胞分化情况,观察NBT阳性细胞数;流式细胞术检测c-myc和c-fos蛋白表达。结果:与空白对照组比较,硒化壳聚糖各组作用与阳性对照组相似,NBT还原阳性细胞明显增多,c-myc蛋白表达显著下降(P<0.01或P<0.05),c-fos蛋白表达显著升高(P<0.01或P<0.05)。结论:硒化壳聚糖可能通过增强HL60细胞c-fos表达及下调c-myc表达来诱导细胞分化。     

硒化壳聚糖对NB_4细胞的周期阻断及与阿霉素的协同作用

目的:研究硒化壳聚糖对人急性早幼粒细胞性白血病细胞株NB4细胞的周期阻断作用及与阿霉素(ADM)合用的协同作用。方法:采用流式细胞术观察药物对细胞的凋亡及周期阻断作用;Western blot法检测细胞中Cyclin D1蛋白含量的变化;MTT法检测硒化壳聚糖与ADM合用对细胞增殖的影响。结果:硒化壳聚糖可阻断细胞于G0~G1期,并呈剂量依赖性地降低细胞中Cyclin D1含量。2药合用对NB4细胞的抑制率高于2药相应浓度单独使用。结论:硒化壳聚糖可能是通过抑制细胞中Cyclin D1的表达,使细胞阻滞于G0~G1期,从而诱导NB4细胞凋亡并抑制其增殖,其与ADM合用有协同抑制NB4细胞增殖作用。     

Growth inhibition and apoptosis of human leukemia K562 cells induced by seleno-short-chain chitosan

In this article, the in vitro effects of seleno-short-chain chitosan (SSCC, molecular weight between 5,000 and 10,000 Da) on the proliferation of human leukemia K562 cells were investigated to illustrate the possible mechanisms involved. 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assays showed that short-chain chitosan significantly suppressed the growth of K562 cells in a dose-dependent and time-dependent manner, although normal mouse embryonic fibroblasts NIH3T3 were viable after the same treatment. Cell growth inhibitory rate could reach 95% after exposure with more than 100 microg/ml SSCC for 72 h. Flow cytometry analysis revealed that treatment of K562 cells with SSCC resulted in the accumulation of cells in the G(2)/M phase. The growth inhibition of K562 cells after treatment with SSCC was subsequently associated with the induction of apoptosis, as evidenced by (1) the typical apoptotic morphologic changes measured by a fluorescence microscope, (2) the internucleosomal DNA fragmentation into a ladder determined by agarose gel electrophoresis and (3) the occurrence of sub-G(0)/G(1) phase cells analyzed by flow cytometry. All these results indicated that SSCC may have therapeutic potential in human leukemia treatment.     

硒化壳聚糖促进体外培养皮肤成纤维细胞增殖

目的研究硒化壳聚糖对体外培养的皮肤成纤维细胞增殖的影响。方法用不同剂量（25、50、100、200、400mg/L）硒化壳聚糖作用于成纤维细胞,光镜下观察药物对细胞形态的影响;MTT法、3H-TdR掺入法、细胞生长动力学研究用于检测药物对细胞增殖影响,LDH漏出率检测药物对细胞增殖及损伤的影响,并以等体积细胞培养液处理为对照组。结果各药物浓度组处理细胞后,细胞形态未见明显改变,均可使细胞吸光度值增加,细胞倍增时间缩短,促进表皮细胞对3H-TdR的掺入（P〈0.05）,降低LDH漏出率（P〈0.05）。结论硒化壳聚糖对体外培养皮肤成纤维细胞增殖具有促进作用。     

Improved cytotoxicity and multidrug resistance reversal of chitosan based polymeric micelles encapsulating oxaliplatin

To overcome the side effects and drug resistance in cancer chemotherapy, oxaliplatin (OXA) was encapsulated in chitosan based polymeric micelles with glycolipid-like structure, which were formed by stearic acid-grafted chitosan oligosaccharide (CSO-SA). CSO-SA with 6.89% amino substituted degree was synthesized in this paper. The critical micelle concentration was about 0.12?mg/mL. CSO-SA micelles with the concentration of 1.0?mg/mL had 34.8?nm number average diameter and +50.8 mV surface potential in the aqueous medium. Thin-film dispersed method mediated by lecithin was chosen to prepare OXA-loaded CSO-SA micelles (CSO-SA/OXA), encapsulation efficiency of which could reach up to about 47%. In vitro anti-tumor activity of CSO-SA/OXA micelles against drug sensitive tumor cells and drug resistant cells was then examined. Using SGC-7901, SKOV3, BEL-7402, K562, and MCF-7 as model drug sensitive tumor cells, the 50% inhibition of cellular growth (IC₅₀) of CSO-SA/OXA micelles could be lowered about 3-6 folds compared to that of free OXA solution. Furthermore, cytotoxicity test of CSO-SA/OXA micelles against MCF-7 and multidrug resistant MCF-7 (MCF-7/Adr) cells presented the reversal activity against MCF-7/Adr cells. The present micelles are a promising carrier candidate for platinum drug to improve the anti-tumor activity.     

洛美利嗪对人白血病细胞K562/ADM多药耐药的逆转作用

目的：研究洛美利嗪(lomerizine，Lom)对人白血病细胞K562／ADM多药耐药逆转作用及机制。方法：使用MTT法检测Lom对K562／ADM多药耐药细胞柔红霉素(DNR)细胞毒性的影响，使用荧光分光光度计和流式细胞术分析Lom对K562／ADM多药耐药细胞胞内P—糖蛋白(P—glycoprotein，P—gp)底物—罗丹明123(rhodamine 123，Rh123)的累积情况。结果：Lom能明显提高DNR对K562／ADM多药耐药细胞的细胞毒作用，并可使胞内Rh123的浓度增加。K562敏感细胞株则不受影响。结论：Lom能显地抑制：K562／ADM多药耐药细胞上P—gp的活性，提高P—gp底物的胞内浓度，并增强其他抗癌药的细胞毒作用。     

Modulation of ATPase activity by cholesterol and synthetic ether lipids in leukemic cells.

Synthetic ether lipids (EL) exert their antiproliferative action on leukemic cells through localization in the plasma membrane with subsequent biochemical effects which are still being elucidated. In the present study, the modulation of membrane-linked ATPase activity was investigated in relation to changes in membrane fluidity of HL60 and K562 human leukemic cells. Incubation of HL60 and K562 cells with EL under non-cytotoxic conditions caused significant membrane fluidization which was related to the membrane cholesterol (CHOL) levels. HL60 cells, which are sensitive to the cytotoxic action of EL, had a lower basal CHOL content. When HL60 cells were loaded with CHOL, Na+, K(+)-ATPase activity was reduced significantly compared to that of untreated cells. In contrast, CHOL-deprived K562 cells had twice the Na+,K(+)-ATPase activity of unmodified K562 cells. Na+K(+)- and Mg(2+)-ATPase activities were stimulated significantly in both cell lines by EL at concentrations lower than 20 microM. This stimulation was greater in cells richer in CHOL, such as K562 cells and CHOL-enriched HL60 cells. In contrast, Na+,K(+)-ATPase in both cell lines was inhibited by EL above 20 microM regardless of the CHOL content. Mg(2+)-ATPase activity was not related to cell CHOL content and was not inhibited by EL above 20 microM.     

N-正辛基-N′-琥珀酰基壳聚糖的制备及其对4种肿瘤细胞的亲和性

目的:以不同分子质量的壳聚糖为原料合成系列的N-正辛基-N′-琥珀酰基壳聚糖,考察其与肿瘤细胞的亲和性,为其作为抗肿瘤药物的靶向载体提供依据。方法:用异硫氰酸荧光素(FITC)对N-正辛基-N′-琥珀酰基壳聚糖进行标记,再分别与人肝癌细胞(HepG2)、人白血病细胞(K562)、人非小细胞肺癌细胞(A549)及人胃癌细胞(BGC)共培养,通过流式细胞仪及酶联免疫检测仪测定N-正辛基-N′-琥珀酰基壳聚糖对肿瘤细胞的亲和性及抑制力。结果:N-正辛基-N′-琥珀酰基壳聚糖对4种肿瘤细胞亲和性明显强于空白细胞株(P＜0．01),并具有一定的肿瘤抑制作用。结论:N-正辛基-N′-琥珀酰基壳聚糖有望作为抗肿瘤药物的靶向载体。