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71.
本文报道给C57小鼠腹腔注射不同剂量1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)后,发现组3(MPTP35 mg/kg,每天一次,共7天)鼠肝匀浆、线粒体和微粒体的膜丙二醛含量明显增加,与对照组相比分别增加70.5%,67%和51.4%(P<0.01),而组1(MPTP 35mg/kg,每4小时一次,共3次)和组2(MPTP35mg/kg,每天一次,共4天)鼠肝丙二醛含量与对照组相近。结果表明MPTP有明显地促进鼠肝脂质过氧化的作用,并与其剂量有关。 相似文献
72.
73.
根据由精氨酸-甘氨酸-天冬氨酸组成的肽能抑制血小板聚集的机制,设计并合成了[5-(4-甲脒-苄基)-2,4-二氧代-咪唑烷-3-基]-乙酰基-L-天冬氨酰-L-缬氨酸(9)。生物试验结果表明:(9)抑制血小板聚集作用最强,其活性以IC_(50)值相比,强于类似物。 相似文献
74.
Leukotriene B4 (LTB4) and the protein kinase C activator, 4-beta-phorbol dibutyrate (PDBu), both induced a pronounced and concentration-dependent stimulation of hydrogen peroxide (H2O2) generation by purified guinea pig peritoneal eosinophils in the concentration range 1 nM-1 microM. The LTB4 response was inhibited competitively by the specific LTB4 receptor antagonist, U-75302, with a KB of 25 nM, while the concentration-response curves for both stimuli were shifted rightwards (3.8-fold and 2.8-fold for LTB4 and PDBu, respectively) by the competitive protein kinase C inhibitor, 1-O-hexadecyl-2-O-methylglycerol at a concentration of 300 microM. LTB4 appears, therefore, to induce respiratory burst in eosinophils via a receptor-mediated mechanism involving protein kinase C. 相似文献
75.
Memantine (1-amino-3,5-dimethyladamantan) was tested as an antagonist of N-methyl-d-aspartate (NMDA) receptors on cultured superior collicular and hippocampal neurones using the patch clamp technique and its actions were compared to those of Mg2+ ions, ketamine, dextrorphan, dextromethorphan, phencyclidine and dizocilpine (MK-801). Memantine (2–33 μM) concentration-dependently antagonized responses to NMDA 100 μM with an IC50 of 2.92 ± 0.05 μM. In contrast, current responses to (S)-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (l-AMPA 50–100 μM) and γ-amino butyric acid (GABA 10 μM) were unaffected by Memantine 8 μM. Memantine 8 μM caused a non-parallel shift of the NMDA concentration-response curve to the right in a manner indicative of uncompetitive open channel block. The effects of memantine were similar to ketamine in that both antagonists were weakly use- and strongly voltage-dependent. In contrast, MK-801, phencyclidine and dextrorphan showed much slower kinetics that was reflected in their marked use- and weaker voltage-dependency. The antagonistic effects of memantine were not reversed by increasing concentrations of glycine (0.1–100 μM) ruling out the possibility of an interaction of memantine with the strychnine-insensitive glycine modulatory site associated with the NMDA receptor-channel complex. Memantine (1–100 μM) also selectively antagonized responses to NMDA (40 μM) in the cortical wedge preparation with IC50 of 12.9 ± 1.5 μM. 相似文献
76.
N┐(4┐乙氧苯基)苯甲酰胺类化合物的合成及抗炎、抗变态反应活性研究周玉新1)党永红刘建飞2)徐颖刘百里(沈阳药科大学制药系,沈阳110015)郑文义(东北第六制药厂,沈阳110043)1981年,刘百里等〔1,2〕发现和研制的新药益肤酰胺,经药理实... 相似文献
77.
KLEOMENIS BARLOS DIMITRIOS GATOS OLGA HATZI NICOLE KOCH SOFIA KOUTSOGIANNI 《Chemical biology & drug design》1996,47(3):148-153
S-4-methoxytrityl cysteine was synthesized and converted into the corresponding Fmoc-Cys(Mmt)-OH by its reaction with Fmoc-OSu. As compared to the corresponding Fmoc-Cys(Trt)-OH, the S-Mmt-function was found to be considerably more acid labile. Quantitative S-Mmt-removal occurs selectively in the presence of groups of the tert butyl type and S-Trt by treatment with 0.5–1.0% TFA. The new derivative was successfully utilized in the SPPS of Tyr1-somatostatin on 2-chlorotrityl resin. In this synthesis groups of the Trt-type were exclusively used for amino acid side-chain protection. Quantitative cleavage from the resin and complete deprotection was performed by treatment with 3% TFA in DCM–TES (95:5) for 30 min at RT. We observed no reduction of tryptophan under these conditions. © Munksgaard 1996. 相似文献
78.
79.
Yossi Gilgun-Sherki Yael Barhum Daphne Atlas Eldad Melamed Daniel Offen 《Journal of molecular neuroscience : MN》1996,27(1):125-135
Accumulating data from experimental studies indicate that oxidative stress has a major role in the pathogenesis of multiple
sclerosis (MS). It has been suggested that local production of reactive oxygen species, probably by macrophages, mediates
axonal damage in both MS patients and the mouse model experimental autoimmune encephalomyelitis (EAE). We have shown previously
that our novel brain-penetrating antioxidant, N-acetylcysteine amide (AD4), reduces the clinical and pathological symptoms, including inflammation and axonal damage in myelin
oligodendrocyte glycoprotein (MOG)-induced chronic EAE in mice. The aim of this study was to examine the molecular mechanism
by which AD4 exerts protection in MOG-induced EAE mice. Therefore, we analyzed gene-expression profile in the spinal cords
of MOG-induced chronic EAE mice and compared them with MOG-induced mice treated with AD4, using a cDNA microarray. We found
that MOG treatment up-regulated genes encoding growth factors, cytokines, death receptors, proteases, and myelin structure
proteins, whereas MOG- and AD4-treated mice demonstrated gene expression profiles similar to that seen in na?ve healthy mice.
In conclusion, our study shows that chronic AD4 administration suppresses the induction of various pathological pathways that
play a role in EAE and probably in MS. 相似文献
80.
Functional effects of the σ ligand, (+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine ((+)-3PPP), were explored in perfused rat tail and rabbit ear arteries in vitro. In the rat tail artery (+)-3PPP inhibited contractile responses to adrenergic nerve stimulation, an effect which was reversed to potentiation by the dopamine D2 receptor antagonist sulpiride. In the rabbit ear artery, however, (+)-3PPP potentiated contractile responses to nerve stimulation, an effect which was unchanged by sulpiride. In the rat tail artery, blockade of norepinephrine uptake by cocaine and deoxycorticosterone in the presence of sulpiride revealed two additional actions of (+)-3PPP. First, an inhibitory action on the monoamine uptake site was confirmed by direct measurement of [3H]norepmephrine accumulation. Second, at higher concentrations, an action to inhibit contractile responses to adrenergic nerve stimulation was manifested at a still unidentified site. These studies demonstrate that the observed functional effect of (+)-3PPP results from its combined actions on three individual sites with the net effect dependent on the relative densities of these different receptor sites in each type of vessel. 相似文献