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201.
The in vitro permeabilities of Caco-2 monolayers and permeabilities in tissue sections from colon of monkey, rabbit, and dog were compared using a series of compounds. The selected compounds differed in their physicochemical properties, such as octanol/water partition coefficient, water solubility, and molecular weight. Their structure included steroids, carboxylic acids, xanthins, alcohols, and polyethylene glycols. A linear permeability relationship was established between Caco-2 and colon tissue from both rabbit and monkey. The results suggest that Caco-2 is twice as permeable as rabbit and five times as permeable as monkey colon. However, no clear relationship could be established between Caco-2 monolayers and dog colon permeability. A relationship between permeability in Caco-2 monolayers and human absorption was found. The results suggest that within certain limits, permeability of Caco-2 monolayers may be used as a predictive tool to estimate human drug absorption. 相似文献
202.
本文以 E.coli CM891为靶细胞,用细菌内抗突变作用模式研究了肉桂醛,鞣酸,二烯丙三硫的抗4NQO 突变性及其作用机制。含质粒 pKM101的 CM891的高抗株(抗50μg/ml 氨苄青霉素)能提高该菌株的自发突变率和4NQO 诱发的突变率以及对鞣酸的杀伤抗性。肉桂醛的抗突变性不依赖质粒 pKM101效应,但与暂时性生长延搁有关。鞣酸及二烯丙三硫的抗突变机制可能包括质粒 pKM101介导的易误修复。上述三种化学物中每二种联合应用均显示抗4NQO 突变性的协同效应及对靶细胞的毒性杀伤作用。 相似文献
203.
强化婴幼儿奶粉中叶酸的测定 总被引:1,自引:0,他引:1
强化叶酸的奶粉在0.05M K_2HPO_4缓冲液中,经均质,调pH4.5,15000g离心20分钟,其清液调pH4.0,进行CGS树脂离子交换层析,用10ml KClK_2HPO_4洗脱,调pH7.0,进行HPLC测定,采用300x3.9mm ODS反相柱,移动相0.05M K_2HPO+MeOH(91+9),流速1ml/分,紫外检测器波长285nm,灵敏度0.0050D。方法相对标准偏差为±3.3%,回收率为87%,最小检测量为0.02μg/ml。 相似文献
204.
本文采用高效液相色谱法测定氨甲环酸中的顺式异构体含量。先用衍生化试剂3,5-二硝基苯酰氯预处理氨甲环酸,然后通过HPLC,以喹啉为内标,YMC-PackAM-302ODS为色谱柱,甲醇-0.02mol/L醋酸铵溶液(4:7)为流动相,在254nm波长处检测,顺式异构体在1~2.5μg/ml范围内线性关系良好(r=0.9961),最低检测限为0.02%。 相似文献
205.
Ye Guoji Machiko Orita Kako Tashiro Hiroko Abe 《Naunyn-Schmiedeberg's archives of pharmacology》1994,349(3):318-323
The effects of glycyrrhetinic acid (GA), an aglycon of glycyrrhizin extracted from the roots of Glycyrrhizae radix, on puromycin aminonucleoside (PA) nephrosis were studied in rats. Urine protein excretion in female rats (130g–150g) receiving PA (50 mg/kg) alone was significantly elevated on the 2nd day after injection of PA and reached a peak on the 14th day. Urinary protein on the 14th day was reduced to 74% in animals treated with GA (20 mg/kg) starting on the 2nd day after injection of PA. The increase in serum cholesterol and the decrease in serum protein were also suppressed by GA. Observation by electron microscopy revealed that the degree of abnormality in glomerular epithelial cells, i.e. loss or fusion of foot processes, was lower in the rats treated with GA after PA injection than in the rat treated with PA alone. Moreover, pretreatment with GA did not suppress urinary protein excretion but when it was given at the same time as PA and after PA a significant decrease in urinary protein excretion was observed.
Correspondence to: H. Abe at the above address 相似文献
206.
An investigation has been made into the effect of 3,4-methylenedioxymethamphetamine (MDMA or ‘Ecstasy’) administration on the concentration of 5-hydroxytryptamine (5-HT), uptake of [3H]5-HT and [3H]paroxetine binding in rat cerebral cortex tissue. Four days after 2 injections of MDMA (20 mg/kg i.p., 6 hr apart) the concentrations of 5-HT and its metabolite 5-HIAA were reduced by 60%. The binding of [3H]paroxetine to the presynaptic 5-HT transporter was decreased and high affinity uptake of [3H]5-HT was reduced by a similar amount, indicating neurodegeneration of 5-HT terminals. Pretreatment with chlormethiazole (100 mg/kg i.p.), 10 min before each MDMA injection prevented the decrease in both [3H]parotextine binding and uptake of [3H]5-HT. The loss in 5-HT and 5-HIAA content was also attenuated. Pretreatment with dizocilpine (1 mg/kg i.p.) or haloperidol (2 mg/kg i.p.) also prevented the MDMA-induced loss of [3H]paroxetine binding and attenuated the loss of 5-HT and 5-HIAA content. All three compounds also decreased the degree of hyperthermia that follows MDMA administration, although previous studies suggest that the long term neurodegeneration is not associated with the acute hyperthermic response. These data support the findings of others that MDMA injection produces degeneration of 5-HT nerve terminals in the cortex, confirm that chlormethiazole, dizocilpine and haloperidol attenuate MDMA-induced neurotoxic loss of 5-HT and demonstrate for the first time that these compounds prevent the neurodegeneration of 5-HT nerve terminals that follows MDMA administration. 相似文献
207.
208.
The effects of arachidonic acid and its metabolites on gamma-aminobutyric acid (GABAA) receptor function were determined in rat cerebral cortical synaptoneurosomes. Incubation of synaptoneurosomes with phospholipase A2 decreased muscimol-induced 36Cl- uptake. Arachidonic acid, the major unsaturated fatty acid released by phospholipase A2, also inhibited muscimol-induced 36Cl uptake. Similar inhibition was obtained with other unsaturated fatty acids (docosahexaenoic, oleic) but not with saturated fatty acids (stearic, palmitic). The effect of arachidonic acid on muscimol responses was inhibited by bovine serum albumin (BSA), and BSA enhanced muscimol responses directly, indicating the generation of endogenous arachidonic acid in the synaptoneurosome preparation. The generation of endogenous arachidonic acid was also indicated by the ability of 2 inhibitors of arachidonic acid metabolism, indomethacin and nordihydroguaiaretic acid (NDGA), to inhibit muscimol-induced 36Cl uptake. We conclude that arachidonic acid probably has both direct and indirect actions on muscimol responses since both enzyme inhibitors inhibited muscimol responses but did not prevent the effect of exogenously added arachidonic acid. In additional experiments, arachidonic acid metabolites generated by cyclooxygenase, prostaglandins D2, E2 and F2 alpha, each decreased muscimol responses; prostaglandins F2 alpha was the most potent inhibitor. Since the unsaturated fatty acids and their metabolites are most susceptible to peroxidation, a generating system of superoxide radicals was tested on muscimol responses. A combination of xanthine and xanthine oxidase inhibited muscimol-induced 36Cl uptake in a concentration-dependent manner. We propose that the inhibition of GABAA neurotransmission by arachidonic acid and its metabolites can lead to increased neuronal excitability. This mechanism may play an important role in the development of neuronal damage following seizures or cerebral ischemia. 相似文献
209.
Claudia Linde Cornelia Löffler Christina Kessler U. Quast 《Naunyn-Schmiedeberg's archives of pharmacology》1997,356(4):467-474
In vascular smooth muscle, openers of ATP-dependent potassium channels (K
ATP channels), such as P1075 (N-cyano-N’-(1,1-dimethylpropyl)-N’’-3-pyridylguanidine), produce relaxation. In this study we have investigated the effects of thiol-modifying agents on the
binding of P1075 and on the 86Rb+ efflux stimulating and vasorelaxant effects of the opener in rat aortic rings. The increase in 86Rb+ efflux induced by P1075 was taken as a qualitative measure of K+ channel opening. The hydrophilic SH-group-oxidizing substance, thimerosal (1 to 100μM), abolished specific binding of [3H]-P1075 with an IC50 value of 7.6±1.2μM; at 30μM, the half time for inhibition was 38min. Two other thiol-oxidizing agents, PMB (4-hydroxy-mercuribenzoic
acid) and DTBNP (2,2’-dithio-bis(5-nitropyridine)), inhibited binding up to 86% and 44%, respectively. The disulphide bond
reducing substance, DTT (1,4-dithiothreitol, 0.1 to 1mM), reduced [3H]-P1075 binding by up to 20% and partially reversed the inhibitory effect of thimerosal. In 86Rb+ efflux experiments, thimerosal (3 to 100μM) concentration-dependently increased basal efflux but inhibited P1075-stimulated
tracer efflux with an IC50 value of 7±1μM. The inhibitory effect occurred with a half-time of approximately 8min and was essentially reversed by DTT.
In rings precontracted with noradrenaline, thimerosal inhibited the vasorelaxant effect in a noncompetitive manner, shifting
the concentration-relaxation curves to the right and reducing maximum relaxation.The data show that oxidation of thiol groups
interferes with the binding of the K
ATP channel opener, P1075; concomitantly, the 86Rb+ efflux stimulating and the vasorelaxant effects are inhibited. Reduction of disulphide bonds by DTT has only minor effects
on the action of P1075. Collectively, the results suggest that intact thiol groups are essential for the functioning of the
KATP channel in rat aorta. The different kinetics governing the inhibition of opener binding and of opener-stimulated 86Rb+ efflux suggest that the SH-groups involved in the two processes differ in their accessibility to thimerosal and/or in their
reactivity.
Received: 7 April / Accepted: 9 July 1997 相似文献
210.
Intestinal intraepithelial lymphocytes (iIEL) are primarily CD8 cells and most of them have a CD28? phenotype, the phenotype of effector cytotoxic T cells. We asked whether the predominance of CD8+ CD28? T cells in the gut may result from peripheral blood T cells preferentially migrating to the iIEL compartment and adhering to iEC. Compared with CD4 cells, adhesion of resting CD8+ T cells to iEC cell lines was significantly higher. Adhesion could be blocked with a MoAb to gp180, a molecule expressed on iEC which is known to interact with CD8/lck. No significant difference in the level of adhesion was observed between CD8+ CD28+ and CD8+ CD28? T cells. Thus CD8 cells may preferentially migrate to the iIEL compartment, but loss of CD28 expression could occur in situ after migration. Consistent with this hypothesis, the CD8+ CD28? cells became enriched after co-culturing T cells with iEC cell lines and primary iEC. Induction of the CD8+ CD28? phenotype in cord blood and adult T cells was observed in co-cultures with iEC and also with mitogens and superantigens. In the latter case, CD28 down-modulation was seen specifically in the Vβ subset targeted by the superantigen, indicating that loss of CD28 expression is a direct result of T cell receptor (TCR)-mediated stimulation. The combined results suggest that CD8+ CD28? T cells are antigen experienced T cells, and that they may have a survival advantage in the presence of gut epithelial cells in vitro. This may contribute to the predominance of CD8+ CD28? T cells in the iIEL compartment. 相似文献