Intravenous ilaprazole is more potent than oral ilaprazole against gastric lesions in rats.

Background And Aims: Ilaprazole is a novel proton pump inhibitor that has been marketed as an oral therapy for acid-related diseases in China and Korea. This study aimed to compare the gastroprotective effects of intravenous and enteral ilaprazole in rat models.

Methods: The rats were divided into 7-8 groups receiving vehicle, esomeprazole, and different doses of intravenous and enteral ilaprazole.

Aquaporin-4 deficiency attenuates opioid dependence through suppressing glutamate transporter-1 down-regulation and maintaining glutamate homeostasis.

Background: Glutamate homeostasis plays a critical role in mediating the addiction-related behaviors. Therefore, preventing the disruption or reestablishing of it is a novel strategy for the treatment of addiction. Glutamate transporters are responsible for clearing extracellular glutamate and maintaining glutamate homeostasis.

[Establishment of isolated rabbit airway smooth muscles responsiveness model for the pharmacodynamic study of anti-rhinoviruses drugs].

Human rhinoviruses (HRVs) are the causative pathogens in more than half of viral upper respiratory tract infections. Currently, no antiviral agents that are active against HRVs are available for clinical use. Because only higher primates are susceptible to HRVs, the screening of new drug is most commonly based on the cell line model.

Agmatine modulates neuroadaptations of glutamate transmission in the nucleus accumbens of repeated morphine-treated rats.

It has been proved that agmatine inhibits opioid dependence, yet the neural mechanism remains unclear. In the present study, the effect of agmatine on the neuroadaptation of glutamate neurotransmission induced by morphine dependence, including changes of the extracellular glutamate level and glutamate receptors in the nucleus accumbens was investigated. We found that agmatine (2.

Comparison of agmatine with moxonidine and rilmenidine in morphine dependence in vitro: role of imidazoline I(1) receptors.

Moxonidine and rilmenidine are classical imidazoline I(1) receptor agonists, and used as anti-hypertension drugs in clinical practice. Agmatine is an imidazoline I(1) receptor endogenous ligand as well as its agonist, but more and more evidences suggest it has no influence on blood pressure. In the present study we compared the effects of moxonidine, rilmenidine and agmatine in the development of morphine dependence, and investigated the role of imidazoline I(1) receptor in the effects of these agents.

Agmatine blocks acquisition and re-acquisition of intravenous morphine self-administration in rats.

Our previous studies showed that agmatine inhibits morphine-induced conditioned place preference, locomotor sensitization and drug discrimination in rats. In the present study, we investigated the effects of agmatine on intravenous morphine self-administration in rats. At a dose of 80 mg/kg/infusion, agmatine did not substitute for intravenous morphine (0.

Aquaporin 4 deficiency modulates morphine pharmacological actions.

Acute administration of opioids produces analgesia, while chronic administration induces tolerance and dependence. Aquaporin 4 (AQP4) is most strongly expressed in astrocytes throughout central nervous system, and plays an important role in some pathophysiological processes in brain. However, whether AQP4 modulates opioid analgesia, tolerance and dependence or not remains unknown.

Effect of agmatine on DAMGO-induced mu-opioid receptor down-regulation and internalization via activation of IRAS, a candidate for imidazoline I(1) receptor.

Agmatine, an endogenous ligand for imidazoline I(1) receptor, has previously been shown to prevent opioid tolerance in rats and mice, but the cellular mechanisms remain unknown. In the present study, the effects of agmatine activation on imidazoline I(1) receptor on the desensitization, down-regulation and internalization of micro opioid receptor were investigated. Two cell lines, CHO cells transfected micro opioid receptor (CHO-micro cells) and co-transfected micro opioid receptor and imidazoline I(1) receptor antisera-selected protein (IRAS) (CHO-micro/IRAS cells), were used.

Agmatine inhibits morphine-induced drug discrimination in rats.

Our previous studies have shown that agmatine inhibited morphine-induced conditioned place preference and locomotor sensitization in rats. In the present study, we further investigated the effects of agmatine on the discriminative stimulating effects produced by morphine in rats. Agmatine, at the dose range of 10-80 mg/kg (i.

Effects of intragastric agmatine on morphine-induced physiological dependence in beagle dogs and rhesus monkeys.

Our previous studies demonstrated that subcutaneous injection of agmatine inhibits tolerance to and physiological dependence on morphine in mice and rats. In the present study we further evaluated the effects of intragastric (i.g.

Analgesic activity of ZC88, a novel N-type voltage-dependent calcium channel blocker, and its modulation of morphine analgesia, tolerance and dependence.

ZC88 is a novel non-peptide N-type voltage-sensitive calcium channel blocker synthesized by our institute. In the present study, the oral analgesic activity of ZC88 in animal models of acute and neuropathic pain, and functional interactions between ZC88 and morphine in terms of analgesia, tolerance and dependence were investigated. In mice acetic acid writhing tests, ZC88 (10-80 mg/kg) administered by oral route showed significant antinociceptive effects in a dose-dependent manner.

Agmatine inhibits morphine-induced locomotion sensitization and morphine-induced changes in striatal dopamine and metabolites in rats.

The effects of agmatine on morphine-induced locomotion sensitization and morphine-induced changes in extracellular striatal dopamine (DA) and DA metabolites were studied. The locomotor response to morphine challenge (3 mg/kg, s.c.

Modulation of agmatine on calcium signal in morphine-dependent CHO cells by activation of IRAS, a candidate for imidazoline I1 receptor.

The present study investigated the effects of agmatine action on imidazoline I1 receptor antisera-selected protein (IRAS), a candidate for imidazoline I1 receptor, on prolonged morphine-induced adaptations of calcium signal and long-lasting alterations in gene expression to further elucidate the role of IRAS in opioid dependence. Two cell lines, Chinese hamster ovary cells expressing mu opioid receptor alone (CHO-mu) and expressing mu opioid receptor and IRAS together (CHO-mu/IRAS), were used. After chronic treatment with morphine for 48 h, naloxone induced a significant elevation of intracellular calcium concentration ([Ca2+]i) in CHO-mu and CHO-mu/IRAS cells.

Involvement of phosphatidylcholine-selective phospholipase C in activation of mitogen-activated protein kinase pathways in imidazoline receptor antisera-selected protein.

Imidazoline receptor antisera-selected protein (IRAS) is considered as a candidate for the I1-imidazoline receptor (I1R), but the signaling pathway mediated by IRAS remains unknown. In our study, the signal transduction pathways of IRAS were investigated in CHO cells stably expressing IRAS (CHO-IRAS), and compared to the native I1R signaling pathways. Rilmenidine or moxonidine (10 nM-100 microM), I1R agonists, failed to stimulate [35S]-GTPgammaS binding in CHO-IRAS cell membrane preparations, suggesting that G protein may not be involved in IRAS signaling pathway.

Inhibition by agmatine on morphine-induced conditioned place preference in rats.

Our previous studies demonstrated the ability of exogenous agmatine to inhibit tolerance to and physical dependence on morphine in mice, rats and monkeys. The present study further evaluated the effect of agmatine on the psychological dependence induced by morphine in conditioned place preference assay. Agmatine (0.

Inhibitory effect of agmatine on proliferation of tumor cells by modulation of polyamine metabolism.

Aim: To assess the inhibitory effect of agmatine on tumor growth in vivo and tumor cell proliferation in vitro.

Methods: The transplanted animal model, [3H]thymidine incorporation assay,3-[4,5-dimethythiazol-2-yl]-2,5-diphenyltetrazolium assay, and lactate dehydrogenase (LDH) release assay were performed.

Results: Agmatine, at doses of 5-40 mg/kg, suppressed the S180 sarcoma tumor growth dose-dependently in mice in vivo and the highest inhibitory ratio reached 31.

Anticonvulsive effect of agmatine in mice.

The present study was designed to examine the effect of agmatine, the decarboxylated product of L-arginine by L-arginine decarboxylase, on convulsion in the mouse maximal electroshock (MES) test and mouse glutamate-induced convulsant test. MES convulsion and glutamate convulsion were respectively induced by an electrical stimulation (110 V, 0.3 s, 8 Hz) and by intracerebroventricular injection of glutamate (0.