巻号一覧
79 巻 (1999)
- 4 号 p. 403-
- 3 号 p. 263-
- 2 号 p. 125-
- 1 号 p. 1-
79 巻, 3 号
選択された号の論文の20件中1～20を表示しています
- |<
- <
- 1
- >
- >|
Reviews
-
Hiroshi Ueda1999 年 79 巻 3 号 p. 263-268
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーAlthough we have obtained a number of pharmacological tools and mutant mice lacking specific genes related to the pain, the distinct molecular basis of the pain-producing mechanism has remained to be fully clarified since we have been using conventional paradigms of the nociception test that may drive multiple endogenous molecules affecting nociception at the same time. Here, I will introduce a new paradigm of the nociception test. In this test, we focused on polymodal C-fibers by measuring noci- ceptive flexor responses induced by the peripheral application of a single species of nociceptive molecule. In addition, we identified the site of drug actions on nociceptor endings by the fact that the nociception was abolished by the intrathecal pretreatment with antisense oligodeoxynucleotide for receptors. Throughout experiments using this paradigm of the nociception test, it was firstly revealed that substance P, a major neurotransmitter of polymodal C-fibers, directly stimulates nociceptor endings through activation of Gq/11 and phospholipase C, followed by Ca2+ influx through plasma membrane-bound inositol trisphosphate receptors, and that bradykinin and histamine, both endogenous representative pain-producing substances, share this mechanism. Another unique mechanism is through Gi-coupled receptors such as receptors for nociceptin (orphanin FQ) or kyotorphin (tyrosine-arginine). The latter mechanism was found to be mediated through a substance P release from nociceptor endings. Future studies including some modifications of this paradigm should be also clinically useful for neuropathic pain research as well as understanding of pain physiology.抄録全体を表示PDF形式でダウンロード (832K)
Regular Papers
-
Naoto Uemura, Koichi Nakamura, Yoko Ishii, Seiichiro Matsukubo, Seiji ...1999 年 79 巻 3 号 p. 269-274
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーTo investigate effects of electrical stimulation on survival days of leukemic mice treated with methotrexate (MTX), L1210-bearing mice were treated by MTX and calcium folinate (leucovorin®) rescue therapy (MTX: 400 mg/kg, followed by leucovorin at the dose of 7.5 mg/kg at 8, 15 and 24 hr after MTX) under electrical stimulation (foot shock: shock amplitude, 0.4 mA; voltage, 60 - 100 V/cm; shock duration, 5 sec; frequency, 0.5 Hz) of various lengths. The survival days were significantly prolonged by 6-hr electrical stimulation in combination with MTX, while plasma MTX concentrations and pharmacokinetic parameters such as the area under the curve (AUC0 - 12 hr) and clearance (CL) were not significantly altered. Psychological stress did not alter the efficacy of MTX in the communication box paradigm. Amplified efficacy of MTX was shown in a length-dependent manner when electrical stimulation of various lengths were applied to L1210-bearing mice.抄録全体を表示PDF形式でダウンロード (868K) -
Junko Kimura, Masanori Kawahara, Eiichi Sakai, Junichi Yatabe, Hironor ...1999 年 79 巻 3 号 p. 275-281
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーWe investigated effects of a novel cardioprotective drug, JTV-519 (4-[3-(4-benzylpiperidin-1-yl)propionyl]-7-methoxy-2, 3, 4, 5-tetrahydro-1, 4-benzothiazepine monohydrochloride) on membrane currents of guinea pig ventricular myocytes by whole-cell voltage and current clamp methods. The fast Na+ current (iNa) was activated by ramp pulses from various holding potentials of -90, -80 or -60 mV to 10 mV with various intervals. At 0.2 Hz, JTV-519 inhibited iNa in a concentration-dependent manner with an IC50 of approximately 1.2 and 2 μM at the holding potential of -60 and -90 mM, respectively, implicating a voltage-dependent block. Increasing the pulse frequency from 1 to 2 or 3.3 Hz in the presence of 1 μM JTV-519 shortened the time-course and increased the level of iNa block, indicating a frequency-dependent block. The time-course of iNa blocking by JTV-519 was slower than that of lidocaine and similar to that of quinidine. Ca2+ current (iCa) and the inwardly rectifying K+ current (iK1) were also inhibited by JTV-519. JTV-519 decreased the duration and the height of the plateau of the action potential. We conclude that JTV-519 has frequency- and voltage-dependent blocking effects on iNa as well as inhibition of iCa and iK1.抄録全体を表示PDF形式でダウンロード (846K) -
Fujiko Sanae, Hisao Hayashi, Keigo Chisaki, Yasuhiro Komatsu1999 年 79 巻 3 号 p. 283-288
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーEffects of Saiko-ka-ryukotsu-borei-to (SRBT) on theophylline-induced tachycardia in anesthetized rats and theophylline-induced locomotion and convulsions in mice were examined. An intraduodenal administration of SRBT (1 g/kg) prevented theophylline (5 mg/kg, i.v.)-induced tachycardia in rats. SRBT also attenuated an increase in arterial blood pressure with a slow reduction in heart rate of rats treated with theophylline, with no influence on the plasma level of theophylline. However, SRBT did not change the beating rate of right atrium isolated from rats in the absence or presence of theophylline or isoproterenol. The locomotor activity of theophylline in mice was reduced by the treatment with SRBT. Furthermore, the latency of convulsions in mice induced by administration of theophylline at a higher dose (240 mg/kg, i.p.) was prolonged by treatment with SRBT (1 g/kg, p.o.) and seven out of fifteen mice were saved from death due to convulsions. These results suggest that theophylline-induced tachycardia and central nervous stimulation are suppressed by SRBT and that SRBT may reduce the undesirable actions of theophylline on the cardiovascular and central nervous systems.抄録全体を表示PDF形式でダウンロード (884K) -
Toshihiro Okamoto, Yoshihisa Nakano, Tomio Yamakawa, Kaoru Hara, Ken-I ...1999 年 79 巻 3 号 p. 289-294
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーInterferon-γ (IFN-γ) transgenic mice strongly express IFN-γ in the liver and develop chronic hepatitis. Furthermore, hepatocyte apoptosis was shown by the TdT-mediated dUTP-biotin nick endlabel- ing method. In the present study, interleukin-1β-converting enzyme (ICE) and CPP32-like protease activ- ities in the liver of IFN-γ transgenic mice were measured, using the synthetic substrates Ac-YVAD-MCA and Ac-DEVD-MCA. Plasma aspartate aminotransferase and alanine aminotransferase activities as well as CPP32-like activity were significantly elevated, while ICE activity was significantly reduced. The addition of the ICE inhibitor Ac-YVAD-CHO to IFN-γ transgenic mouse liver cell cytosol had no effect on the CPP32 activity, in contrast to a CPP32 inhibitor. The present results indicate that chronic hepatitis in the IFN-γ transgenic mouse is associated with a decrease in ICE and induction of CPP32-like activity.抄録全体を表示PDF形式でダウンロード (908K) -
Yuji Omiya, Kazuhiro Goto, Yasuyuki Suzuki, Atsushi Ishige, Yasuhiro K ...1999 年 79 巻 3 号 p. 295-301
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーThe analgesia-producing mechanism of processed Aconiti tuber was examined using rodents whose nociceptive threshold was decreased by loading repeated cold stress (RCS). The antinociceptive effect of processed Aconiti tuber (0.3 g/kg, p.o.) in RCS-loaded mice was antagonized by pretreatment with a κ-opioid antagonist, nor-binaltorphimine (10 mg/kg, s.c.), and was abolished by an intrathecal injection of anti-dynorphin antiserum (5 μg). The Aconiti tuber-induced antinociception was inhibited by both dexamethasone (0.4 mg/kg, i.p.) and a dopamine D2 antagonist, sulpiride (10 mg/kg, i.p.), in RCS-loaded mice, and it was eliminated by both an electric lesion of the hypothalamic arcuate nucleus (HARN) and a highly selective dopamine D2 antagonist, eticlopride (0.05 μg), administered into the HARN in RCS-loaded rats. These results suggest that the analgesic effect of processed Aconiti tuber was produced via the stimulation of κ-opioid receptors by dynorphin released in the spinal cord. It was also shown that dopamine D2 receptors in the HARN were involved in the expression of the analgesic activity of processed Aconiti tuber.抄録全体を表示PDF形式でダウンロード (848K) -
Masahiro Ohsawa, Junzo Kamei1999 年 79 巻 3 号 p. 303-311
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーThe involvement of cyclic AMP-dependent protein kinase (PKA) and protein kinase C (PKC) in the modulation of naloxone-precipitated withdrawal jumping in morphine-dependent mice by diabetes was examined. Naloxone-precipitated withdrawal jumps were significantly less in morphine-dependent diabetic mice than in morphine-dependent non-diabetic mice. I.c.v. pretreatment with either calphostin C, a PKC inhibitor, or KT-5720, a PKA inhibitor, attenuated naloxone-precipitated withdrawal jumps in morphine-dependent non-diabetic mice. However, naloxone-precipitated withdrawal jumps in morphinedependent diabetic mice were not attenuated by i.c.v. pretreatment with either calphostin C or KT5720. Moreover, i.c.v. pretreatment with phorbol-12, 13-dibutyrate (PDBu), a PKC activator, attenuated naloxone-precipitated withdrawal jumps in morphine-dependent non-diabetic mice, but not in morphine-depend- ent diabetic mice. The noradrenaline (NA) turnover in the frontal cortex in morphine-dependent non-dia- betic mice, but not in morphine-dependent diabetic mice, was significantly increased 5 min after adminis- tration of naloxone. Naloxone-induced enhancement of NA turnover in morphine-dependent non-diabetic mice, but not in morphine-dependent diabetic mice, was blocked by i.c.v. pretreatment with either calphostin C or KT5720 1 hr before naloxone challenge and blocked by PDBu 1 hr before the last injection of morphine. These results suggest that the co-activation of PKC and PKA is needed to elicit naloxone-precipitated withdrawal jumps and enhancement of turnover rate of NA in the frontal cortex in morphine-dependent non-diabetic mice. Furthermore, the attenuation of naloxone-precipitated withdrawal jumps in morphine-dependent diabetic mice may be due, in part, to the desensitization of μ-opioid receptors by the activation of PKC.抄録全体を表示PDF形式でダウンロード (1363K) -
Hidetoshi Asai, Kiyoshi Kinoshita, Michio Yamamura, Yuzo Matsuoka1999 年 79 巻 3 号 p. 313-317
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーIn order to analyze the receptor properties of central nervous system (CNS)-stimulant thyrotropin-releasing hormone (L-pyroglutamyl-L-histidyl-L-prolinamide, TRH), we evaluated the binding of TRH and its analog taltirelin hydrate ((-)-N-[(S)-hexahydro-1-methyl-2, 6-dioxo-4-pyrimidinylcarbonyl]-L-histidyl-L-prolinamide tetrahydrate; taltirelin, TA-0910) in rat anterior pituitary and several brain regions. There was a specific binding of [3H]methyl TRH (MeTRH) in the anterior pituitary, hypothalamus, brain stem, cerebral cortex and cerebellum with Kd values of 1.0 - 1.6 nM. The inhibition of [3H]MeTRH binding by TRH and taltirelin was monophasic in the anterior pituitary, hypothalamus and brain stem with Ki values of 6.3 - 8.0 nM and 145.5 - 170.4 nM for TRH and taltirelin, respectively. In contrast, the biphasic inhibition was revealed in the cerebral cortex and cerebellum. The Ki values for TRH and taltirelin were 4.1 - 4.3 nM and 67.8 - 73.4 nM for the high affinity binding site and 3.6 - 4.2 μM and 82.3 - 197.5 μM for the low affinity binding site, respectively. Addition of 100 μM GTP or its analog 5′-guanylylimidodiphosphate (Gpp[NH]p) affected neither the biphasic inhibition by TRH nor that by taltirelin. Thus the results suggest the presence of distinct high and low affinity TRH receptors in the CNS in contrast to the pituitary.抄録全体を表示PDF形式でダウンロード (595K) -
Yoshihisa Nagase, Muneshige Kaibara, Yasuhito Uezono, Futoshi Izumi, K ...1999 年 79 巻 3 号 p. 319-325
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーThe effects of propofol, 2, 6-diisopropylphenol, an intravenous general anesthetic, on signal transduction mediated by the rat M1 muscarinic acetylcholine (ACh) receptor (M1 receptor) were examined in electrophysiological studies by analyzing receptor-stimulated, Ca2+-activated Cl--current responses in the Xenopus oocyte expression system. In oocytes expressing the M1 receptor, ACh induced the Ca2+activated Cl- current, in a dose-dependent manner (EC50=114 nM). Propofol (5 - 50 μM) reversibly and dose-dependently inhibited induction of the Ca2+-activated Cl- current by ACh (100 nM) (IC50=5.6 μM). To determine a possible site affected by propofol in this signal transduction, we tested the effects of this anesthetic (10 μM) on the activation of current by injection of CaCl2 and aluminum fluoride (AlF4-). Propofol did not affect activation of the current by the intracellular injected Ca2+, or activation of the current by the intracellular injected AlF4-. These results indicate that propofol does not affect G protein, the inositol phosphate turnover, release of Ca2+ from Ca2+ store or the Ca2+-activated Cl- channel. Propofol apparently inhibits the M1 receptor-mediated signal transduction at the receptor site and/or the site of interaction between the receptor and associated G protein.抄録全体を表示PDF形式でダウンロード (856K) -
Hiroaki Nishijima, Ryuji Uchida, Kimiko Kameyama, Nozomi Kawakami, Tsu ...1999 年 79 巻 3 号 p. 327-334
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーThe inhibitory actions of eugenol on intracellular Ca2+ concentration ([Ca2+]i) and the contractions induced by excess extracellular K+ concentration ([K+]o) in rabbit thoracic aorta were investigated. Application of excess [K+]o solution (30 - 90 mM) produced contraction and increased the intensity of the Ca2+ fluorescence signal. Pretreatment with eugenol (≥0.1 mM) reduced both the amplitude of contraction and the intensity of the Ca2+ fluorescence signal, but the contraction was more strongly affected than the [Ca2+]i. Application of eugenol (0.3 mM) to tissue precontracted by 90 mM [K+]o solution (immediately after the removal of the 90 mM [K+]o solution) slowed the decay of the [Ca2+]i signal, but it did not change the rate of relaxation. Carbonyl cyanide m-chlorophenylhydrozone (10 μM), a mitochondrial metabolic inhibitor, produced a reduction in tension despite a slight increase in [Ca2+]i when applied to muscle precontracted by 90 mM [K+]o solution. These results indicate that eugenol relaxes the rabbit thoracic aorta while suppressing the Ca2+-sensitivity and both the uptake and extrusion mechanisms for Ca2+. To judge from the similarities between its actions and those of metabolic inhibitors, eugenol may produce its actions at least partly through metabolic inhibition.抄録全体を表示PDF形式でダウンロード (870K) -
Kazuki Nakamura, Yu Yamaguchi, Satomi Kagota, Young Mi Kwon, Kazumasa ...1999 年 79 巻 3 号 p. 335-341
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーWe investigated the effect of the water extract of Cordyceps sinensis (WECS) on liver metastasis of Lewis lung carcinoma (LLC) and B16 melanoma (B16) cells in mice. C57BL/6 mice were given a s.c. injection of LLC and B16 cells and sacrificed 20 and 26 days after tumor inoculation, respectively. WECS was daily administered p.o. to the mice in a dose of 100 mg/kg body weight (wt.) in the experiment of LLC and in a dose of 100 or 200 mg/kg body wt. in the experiment of B16 from one week before tumor inoculation to one day before the date of sacrifice. The tumor cells increased in the thigh in LLC-inoculated mice and in the footpad in B16-inoculated mice. The relative liver wt. of the tumor-inoculated mice significantly increased as compared to that of the normal mice due to the tumor metastasis, as verified by the hematoxylin-eosin staining pathological study in the LLC experiment. The relative liver wt. of the WECS-administered mice significantly decreased relative to that of the control mice in both the LLC and B16 experiments. WECS showed a strong cytotoxicity against LLC and B16 cells, while cordycepin (3′-deoxy- adenosine), an active component of WECS, was not cytotoxic against these cells. These findings suggest that WECS has an anti-metastatic activity that is probably due to components other than cordycepin.抄録全体を表示PDF形式でダウンロード (952K) -
Makoto Murakami, Naofumi Tokutomi, Yoshiko Tokutomi, Kimio Tomita, Kat ...1999 年 79 巻 3 号 p. 343-350
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーWe have recently found that mouse megakaryocytes responded to extracellular alkalinization to pH>8.0, generating a K+ current under voltage-clamped conditions with the whole cell recording mode of the patch-clamp technique. The purpose of this study was to physiologically and pharmacologically characterize the alkaline-dependent K+ conductance of the megakaryocyte membrane. The alkalinization-induced K+ current (IALK) did not seem to be Ca2+-dependent since IALK was allowed to be generated under intracellularly Ca2+-buffered conditions with 10 mM EGTA, which completely prevented the generation of caffeine-induced Ca2+-activated currents of mouse megakaryocytes; and no [Ca2+]i elevation was evoked by the alkalinization protocol in contrast to a significant increase in [Ca2+]i in response to caffeine when [Ca2+]i was measured with a fura 2 ratiometry. IALK was strongly suppressed with tetraethylammonium (TEA), 4-aminopyridine (4-AP) and streptomycin (SM), but was completely resistant to quinidine (QND). The values of IC50 for the suppression of IALK with TEA, 4-AP and SM were 5.6, 0.47 and 1.5 mM, respectively. Voltage-gated K+ currents (IK) of the same megakaryocyte preparation were weakly suppressed with TEA and 4-AP, while they were significantly suppressed with either SM or QND. These results suggest that mouse megakaryocytes possess K+ conductance that was activated by extracellular alkalinization and that probably differs from conventional K+ conductance in its pharmacological properties.抄録全体を表示PDF形式でダウンロード (1003K) -
Kimihiro Okubo, Ruby Pawankar, Minoru Gotoh, Toshiaki Yagi1999 年 79 巻 3 号 p. 351-357
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーAllergic reaction of the nose comprises of an immediate and a late reaction. To evaluate nasal allergic reactions, many experiments have been performed by investigators. In this study, we performed a new tissue culture technique (adhesive explant culture) to analyze the migration of cells into the culture medium from the cultured allergic nasal mucosa in response to an allergen. Basophilic cells (mast cells and basophils) and eosinophils, which were released into the culture medium after the allergen challenge, were evaluated by the analysis of histamine and eosinophil cationic protein (ECP) content in the culture medium. Histamine and basophilic cells in the culture medium were more abundant in the immediate phase (within 30 min) after challenge than in the late phase (from 30 min to 10 hr). On the other hand, ECP and eosinophils in the culture medium were more abundant in the late phase than in the immediate phase. The increase of histamine content in both phases were not inhibited by pre-treatment of emedastine difumarate (EME), an anti-allergic drug. However, the increase of ECP in the late phase was inhibited by pre-treatment with EME. Moreover, the number of EG2-positive cells was also decreased by pre-treatment with EME. These results suggest that EME might lower the activation of eosinophils in the late phase of the allergic reaction. The present study also indicates that this adhesive explant culture system is useful model for studying the cellular allergic responses to drugs ex vivo.抄録全体を表示PDF形式でダウンロード (952K) -
Yoshito Fujiseki, Kyoko Omori, Koichiro Omori, Yoshito Mikami, Junko S ...1999 年 79 巻 3 号 p. 359-368
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーWe tried to detect natriuretic peptide (NP) receptor (NPR-A and NPR-B) mRNAs in cultured rabbit retinal pigment epithelium (RPE) cells and examined the regulation of their expression in relation to subretinal fluid absorption or RPE cell proliferation. RPE cells from 2 - 4 passages were grown to confluence on microporous membranes and analyzed for levels of expression of receptor mRNAs by quantitative RT-PCR and Northern blotting. The expression of NPR-B mRNA was approximately tenfold higher than that of NPR-A mRNA. The expression of NPR-A mRNA was not affected by treatments that may change subretinal fluid transport, while that of NPR-B mRNA was inhibited by transmitters involved in light- and dark-adaptation such as dopamine and melatonin. Expression of NPR-B mRNA was also suppressed by platelet-derived growth factor and transforming growth factor-β. Furthermore, atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP), ligands for NPR-A and B, respectively, inhibited the proliferation of RPE cells, as analyzed by incorporation of [3H]thymidine. These findings suggest that ANP may be involved in constitutive absorption of subretinal fluid and that NPs form an important regulatory system of proliferation in RPE cells.抄録全体を表示PDF形式でダウンロード (1437K) -
Jun Harada, Masahiko Sugimoto1999 年 79 巻 3 号 p. 369-378
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーBoth p38 mitogen-activated protein kinase (p38) and c-Jun N-terminal kinase (JNK) are known to play important roles in neuronal apoptosis. However, the relationship between these kinases and caspases, another key mediator of apoptosis, is unclear. In the present study, we investigated the possible effects of SB203580 [(4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)-imidazole), an inhibitor of p38, on caspase activation and apoptosis of cultured rat cerebellar granule neurons. In granule neurons, SB203580 prevented apoptosis that was induced by lowering the concentration of KCl in the culture medium for 24 hr. SB203580 also prevented augmentation of caspase-3-like protease activity at 8 hr after the low KCl treatment. The IC50 values of SB203580 for both events were between 3 μM and 10 μM. Expression and phosphorylation of c-Jun, potently induced by low KCl treatment, were prevented by SB203580 at 10 μM. Z-Asp-CH2-DCB, a caspase inhibitor with anti-apoptotic activity, did not inhibit the induction and phosphorylation of c-Jun. Granule neurons displayed high levels of p38 and JNK activities. SB203580 inhibited not only p38 but also JNK activities extracted from granule neurons. These results suggest that activation of c-Jun by p38 and/or JNK mediates the activation of caspase in the low KCl-induced apoptosis in cerebellar granule neurons.抄録全体を表示PDF形式でダウンロード (1494K) -
Takaya Nitta, Tohru Fukushima, Hiromichi Nakamuta, Masao Koida1999 年 79 巻 3 号 p. 379-386
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーPreviously we reported that 8-week treatment with methylprednisolone acetate (MPA: 0.1 mg/kg, s.c., 3 days a week) of male rats caused a novel type of osteopenia whose development was prevented by salmon calcitonin (SCT) in a dose-dependent manner. In this study, to compare the MPAinducible osteopenia with the ovariectomy (OVX)-inducible one, female rats were used instead of male rats and a time-course study of development was made. MPA treatments for 1, 2, 4 and 8 weeks histologically induced characteristic osteopenic changes in a time-dependent manner that were histomorphometrically detectable in tibiae within 4 weeks as reduced bone mass, accelerated bone resorption, and suppressed bone formation and mineralization. Node-strut analysis revealed that the connectivity of the trabecular structure remained unaffected. Such MPA-induced changes in the trabecular structure, to be defined as thinned-but-uncut, is in a good contrast with OVX-induced unthinned-but-cut structure, although the latter osteopenic changes became detectable 2 weeks earlier. Another previous finding confirmed herein was that MPAinduced osteopenia in female rats was also completely masked by SCT (10 U/kg, s.c., 5 days a week). The results indicate that the MPA-inducible secondary osteopenic model in either sex of rats would be usable for testing anti-osteopenic drugs.抄録全体を表示PDF形式でダウンロード (1078K)
Short Communications
-
Yasuyuki Suzuki, Kazuhiro Goto, Atsushi Ishige, Yasuhiro Komatsu, Junz ...1999 年 79 巻 3 号 p. 387-391
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーUsing streptozotocin-induced diabetic mice and rats, we evaluated the antinociceptive mechanism of Gosha-jinki-gan. The antinociceptive effect of Gosha-jinki-gan (0.3 g/kg, p.o.) in diabetic mice, as determined by the tail-pressure test, was inhibited by NG-nitro-L-arginine methyl ester (L-NAME; 2, 5 mg/kg, i.p.). When L-NAME (10 μg) or methylene blue (500 μg) was topically administered to the intraplantar area of the hind paw, the region used for the paw-pressure test, the antinociceptive activity of Gosha-jinki-gan (0.3 g/kg, p.o.) in diabetic rats was decreased. These results suggested that the antinociceptive effect of Gosha-jinki-gan partly resulted from the peripheral action of increasingly produced nitric oxide.抄録全体を表示PDF形式でダウンロード (704K) -
Takeshi Kihara, Shun Shimohama, Akinori Akaike1999 年 79 巻 3 号 p. 393-396
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーPreviously we demonstrated that nicotinic acetylcholine receptor stimulation protects neurons against beta-amyloid (Aβ)-induced cytotoxicity. In the present study, the effects of nicotinic receptor agonists on the β-sheet formation were investigated using a thioflavin T (ThT)-based fluorescence assay. Nicotine, cytisine (an α4β2 agonist), and 3-(2, 4)-dimethoxybenzylidene anabaseine (DMXB, an α7 agonist) did not reduce fluorescence intensity when these agents were added to the β-sheet-formed Aβ. Simultaneous incubation of Aβ with nicotinic agonists also did not cause a reduction in fluorescence intensity. This data suggests that nicotinic receptor agonists do not influence the formation of the β-sheet structure.抄録全体を表示PDF形式でダウンロード (468K) -
Naoto O’uchi, Haruko Nishikawa, Hiroyuki Motoie, Hisataka Shikam ...1999 年 79 巻 3 号 p. 397-400
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーWe examined mechanisms by which incadronate disodium (YM175) prevented bone resorption in ovariectomized dogs with dietary calcium restriction using the morphometrical method. YM175 (0.01-1.0 mg/kg) was given to ovariectomized dogs for 18 months. Because lumbar bone mineral density remained constant at month 17, we assumed that the trabecular bone resorption rate was equal to the bone formation rate and that wall thickness equaled resorption cavity depth. YM175 decreased both the bone resorption rate per number of osteoclasts and resorption cavity depth of cancellous pockets which were increased in ovariectomized dogs. These results suggest that YM175 reduces bone loss by decreasing the resorbing activity of osteoclasts.抄録全体を表示PDF形式でダウンロード (517K) -
Keiichi Musoh, Kayoko Kawamura, Isao Miyake, Shino Shimada, Tetsuo Oha ...1999 年 79 巻 3 号 p. 401-402
発行日: 1999年
公開日: 2001/03/31
ジャーナル フリーThe objective of the present study was to determine the action duration of tulobuterol tape within a 24-hr period in conscious guinea pigs. The bronchoconstriction induced by histamine-inhalation was significantly inhibited by tulobuterol tape in comparison with its placebo tape 8 and 12 hr after binding, and the inhibitory rate was 50±11% and 35±13%, respectively. Twenty-four hours after binding, the inhibitory effect of tulobuterol tape gradually diminished, but the inhibitory rate was maintained at 30±14%. These results suggests that tulobuterol tape has a long lasting bronchodilatory action.抄録全体を表示PDF形式でダウンロード (268K)
- |<
- <
- 1
- >
- >|