sincalide and 1-(4-bromophenylaminocarbonyl)-4-5-diphenyl-3-pyrazolidinone
sincalide has been researched along with 1-(4-bromophenylaminocarbonyl)-4-5-diphenyl-3-pyrazolidinone* in 3 studies
Other Studies
3 other study(ies) available for sincalide and 1-(4-bromophenylaminocarbonyl)-4-5-diphenyl-3-pyrazolidinone
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Cholecystokinin octapeptide regulates the differentiation and effector cytokine production of CD4(+) T cells in vitro.
Cholecystokinin octapeptide (CCK-8), an immunomodulatory peptide, can promote or suppress the development or function of specific CD4(+) T cell subsets by regulating antigen-presenting cell functions. In the current study, we investigated whether CCK-8 exerts a direct effect on T cells through influencing differentiation and cytokine production of distinct CD4(+) T cell subsets in vitro. Our results showed that CCK-8 differentially affects the development and function of CD4(+) T cell populations, with a negative influence on Th1 and Th17 cells and positive regulatory effect on inducible T regulatory cells (iTreg). Notably, CCK-8 suppressed Th1 while slightly enhancing Th2 development and cytokine production. Similarly, CCK-8 inhibited the differentiation of Th17 cells and promoted Foxp3 expression. L-364,718 and LY-288,513, selective antagonists of CCK1R and CCK2R, respectively, suppressed the effects of CCK-8 on CD4(+) T cell subset-specific transcription factors. Our findings strongly indicate that CCK-8 exerts a direct effect on T cells, which is dependent on CCKRs, particularly CCK2R. The collective results aid in further clarifying the mechanism underlying the anti-inflammatory and immunoregulatory effects of CCK-8. Topics: Animals; Anti-Inflammatory Agents; CD4-Positive T-Lymphocytes; Cell Differentiation; Cells, Cultured; Devazepide; Forkhead Transcription Factors; In Vitro Techniques; Lymphocyte Activation; Mice; Mice, Inbred C57BL; Pyrazoles; Receptor, Cholecystokinin A; Receptor, Cholecystokinin B; Sincalide; T-Lymphocyte Subsets; T-Lymphocytes, Regulatory; Th1 Cells; Th17 Cells; Th2 Cells | 2014 |
Effects of exogenous cholecystokinin octapeptide on acquisition of naloxone precipitated withdrawal induced conditioned place aversion in rats.
Cholecystokinin octapeptide (CCK-8), a gut-brain peptide, regulates a variety of physiological behavioral processes. Previously, we reported that exogenous CCK-8 attenuated morphine-induced conditioned place preference, but the possible effects of CCK-8 on aversively motivated drug seeking remained unclear. To investigate the effects of endogenous and exogenous CCK on negative components of morphine withdrawal, we evaluated the effects of CCK receptor antagonists and CCK-8 on the naloxone-precipitated withdrawal-induced conditioned place aversion (CPA). The results showed that CCK2 receptor antagonist (LY-288,513, 10 µg, i.c.v.), but not CCK1 receptor antagonist (L-364,718, 10 µg, i.c.v.), inhibited the acquisition of CPA when given prior to naloxone (0.3 mg/kg) administration in morphine-dependent rats. Similarly, CCK-8 (0.1-1 µg, i.c.v.) significantly attenuated naloxone-precipitated withdrawal-induced CPA, and this inhibitory function was blocked by co-injection with L-364,718. Microinjection of L-364,718, LY-288,513 or CCK-8 to saline pretreated rats produced neither a conditioned preference nor aversion, and the induction of CPA by CCK-8 itself after morphine pretreatments was not significant. Our study identifies a different role of CCK1 and CCK2 receptors in negative affective components of morphine abstinence and an inhibitory effect of exogenous CCK-8 on naloxone-precipitated withdrawal-induced CPA via CCK1 receptor. Topics: Animals; Conditioning, Psychological; Devazepide; Male; Morphine Dependence; Naloxone; Pyrazoles; Rats; Rats, Wistar; Receptors, Cholecystokinin; Sincalide; Spatial Behavior; Substance Withdrawal Syndrome | 2012 |
CCK-A and CCK-B selective receptor agonists and antagonists modulate olfactory recognition in male rats.
Modulation of learning and memory is one of the physiological roles that the neuropeptide cholecystokinin (CCK-8) may play. We have used a behavioural model of olfactory recognition among rats to test this hypothesis and to explore the relationship between CCK-A and CCK-B receptors and memory retention. Adult male rats form a transient memory of a juvenile congenere as indicated by a reduction in the duration of investigatory behaviour upon re-exposure 30 min after an initial exposure, but not when re-exposure is delayed until 120 min afterwards. In the present study, rats were treated after the first contact with various compounds; inhibition and facilitation of olfactory recognition were evaluated as the persistence in investigation 30 min and the decrease in investigation 120 min after pharmacological manipulations, respectively. Systemic injection of CCK-8, of a selective CCK-A agonist, or of non-peptide CCK-B antagonists (CI-988 and LY-262691) enhanced olfactory recognition. In contrast, the CCK-B selective agonist BC 264 and the tetrapeptide CCK-4 both disrupted it. Taken together with previous evidence of the detrimental effect of the nonpeptide. CCK-A antagonist devazepide on olfactory recognition, these results confirm and extend the hypothesis that there is a balance between CCK-A-mediated facilitative effects and CCK-B-mediated inhibitory effects on memory retention. Topics: Amino Acid Sequence; Animals; Benzodiazepinones; Cholecystokinin; Cognition; Indoles; Male; Meglumine; Molecular Sequence Data; Peptide Fragments; Phenylurea Compounds; Pyrazoles; Rats; Rats, Wistar; Receptors, Cholecystokinin; Sincalide; Smell; Social Behavior | 1994 |