• Korean Journal of Plant Resources
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• v.23 no.6
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• pp.513-518
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• 2010

In the present study, the antinociceptive profiles of Dianthus chinensis L extract were examined in ICR mice. Dianthus chinensis L extract administered orally (200 mg/kg) showed an antinociceptive effect as measured by the tail-flick and hot-plate tests. In addition, Dianthus chinensis L extract attenuated the writhing numbers in the acetic acid-induced writhing test. Furthermore, the cumulative nociceptive response time for intrathecal (i.t.) injection of substance P ($0.7\;{\mu}g$) was diminished by Dianthus chinensis L extract. Intraperitoneal (i.p.) pretreatment with yohimbine ($\alpha_2$-adrenergic receptor antagonist) attenuated antinociceptive effect induced by Dianthus chinensis L extract in the writhing test. However, naloxone (opioid receptor antagonist) or methysergide (5-HT serotonergic receptor antagonist) did not affect antinociception induced by Dianthus chinensis L extract in the writhing test. Our results suggest that Dianthus chinensis L extract shows an antinociceptive property in various pain models. Furthermore, this antinociceptive effect of Dianthus chinensis L extract may be mediated by $\alpha_2$-adrenergic receptor, but not opioidergic and serotonergic receptors.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.6
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• pp.295-300
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• 2004

Serotonin (5-hydroxytroptamine, 5-HT) has been shown to affect the induction of long-term potentiation (LTP) in the cortex such as the hippocampus, the visual cortex and the prefrontal cortex. Fluoxetine, as a selective serotonin reuptake inhibitor, is used in the management of a wide variety of psychological diseases. To study the effect of fluoxetine on the induction of LTP, we recorded the field potential in layer II/III of the frontal cortex from 3-wk-old. LTP was induced in horizontal input by theta burst stimulation (TBS). TBS with two-folds intensity of the test stimulation induced LTP, which was blocked by application of D-AP5 $(50 {\mu}M)$, an NMDA receptor antagonist. Whereas bath application of 5-HT $(10 {\mu}M)$ inhibited the induction of LTP, treatment with the 5-HT depleting agent, para-chloroamphetamine $(PCA,\;10{\mu}M)$, for 2hr did not affect the induction of LTP. Bath application of fluoxetine (1, 3, and $10 {\mu}M)$ suppressed the induction of LTP in concentration-dependent manner, however, fluoxetine did not inhibit the induction of LTP in 5-HT-depleted slices. These results indicate that fluoxetine may inhibit the induction of LTP by modulating serotonergic mechanism in the rat frontal cortex.

• Korean Journal of Biological Psychiatry
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• v.8 no.2
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• pp.208-219
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• 2001

The pharmacotherapy of schizophrenia exhibits wide inter-individual variabilities in clinical efficacy and adverse effects. Recently, human genetic diversity has been known as one of the essential factors to the variation in human drug response. This suggests that drug therapy should be tailored to the genetic characteristics of the individual. Pharmacogenetics is the field of investigation that attempts to elucidate genetic basis of an individual's responses to pharmacotherapy, considering drug effects divided into two categories as pharmacokinetics and pharmacodynamics. The emerging field of pharmacogenomics, which focuses on genetic determinants of drug response at the level of the entire human genome, is important for development and prescription of safer and more effective individually tailored drugs and will aid in understanding how genetics influence drug response. In schizophrenia, pharmacogenetic studies have shown the role of genetic variants of the cytochrome P450 enzymes such as CYP2D6, CYP2C19, and CYP2A1 in the metabolism of antipsychotic drugs. At the level of drug targets, variants of the dopamine $D_2$, $D_3$ and $D_4$, and 5-$HT_{2A}$ and 5-$HT_{2C}$ receptors have been examined. The pharmacogenetic studies in schizophrenia presently shows controversial findings which may be related to the multiple involvement of genes with relatively small effects and to the lack of standardized phenotypes. For further development in the pharmacogenomics of schizophrenia, there would be required the extensive outcome measures and definitions, and the powerful new tools of genomics, proteomics and so on.

• Journal of Life Science
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• v.25 no.5
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• pp.515-522
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• 2015

Treculia africana Decne, a breadfruit species, is native to many parts of West and Tropical Africa. The breadfruit belongs to the family Moraceae and is one of the four members of the genera Treculia. The crude extract of T. africana has been used in folk medicine as an anti-inflammatory agent for various ailments, such as whooping cough. In this study, we evaluated the anti-oxidative and anti-cancer activities of the methanol extract of T. africana Decne (META) and the molecular mechanisms of its anti-cancer effects in human colon carcinoma HT29 cells. The META exhibited anti-oxidative activity through a DPPH radical scavenging capacity and inhibited cell growth in a dose-dependent manner in HT29 cells. META treatment induced apoptosis of HT29 cells, showing an increase in the percentage of both SubG1 cells and Annexin V-positive cells and the formation of apoptotic bodies in a dose-dependent manner. META-mediated apoptosis was associated with the up-regulation of the death receptor FAS and Bax and a decrease in the Bcl-2 expression. META-treated HT29 cells also showed the release of cytochrome c from the mitochondria into the cytosol, activation of caspase-3, caspase-8, and caspase-9, and proteolytic cleavage of poly ADP-ribose polymerase (PARP). These findings suggest META may exert an anti-cancer effect in HT29 cells by inducing apoptosis through both intrinsic and extrinsic pathways.

• Journal of Ginseng Research
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• v.29 no.1
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• pp.19-26
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• 2005

The last two decades have shown a marked expansion in publications of diverse effects of Panax ginseng. Ginsenosides, as active ingredients of Panax ginseng, are saponins found in only ginseng. Recently, a line of evidences shows that ginsenosides regulate various types of ion channel activity such as $Ca^{2+},\;K^+,\;Na^+,\;Cl^-$, or ligand gated ion channels (i.e. $5-HT_3$, nicotinic acetylcholine, or NMDA receptor) in neuronal, non-neuronal cells, and heterologously expressed cells. Ginsenosides inhibit voltage-dependent $Ca^{2+},\;K^+,\;and\;Na^+$ channels, whereas ginsenosides activate $Ca^{2+}-activated\;Cl^-\;and\;Ca^{2+}-activated\;K^+$ channels. Ginsenosides also inhibit excitatory ligand-gated ion channels such as $5-HT_3$, nicotinic acetylcholine, and NMDA receptors. This review will introduce recent findings on the ginsenoside-induced differential regulations of ion channel activities and will further expand the possibilities how these ginsenoside-induced ion channel regulations are coupled to biological effects of Panax ginseng.

• Korean Journal of Biological Psychiatry
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• v.3 no.1
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• pp.121-126
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• 1996

Objects : There is considerable interest in the role of serotonin(5-HT) in the pathophysiology of schizophrenia. Cimetidine, $H_2$ antagonist, produces transient increase in serum prolactin(PRL) levels by indirect serotonergic mechanism in man following intravenous administration. Therefore the authors investigated the effects of cimetidine on serum PRL levels of male unmedicated schizophrenics. Method : Baseline serum prolactin level and psychopathology were measured at 9:00 AM. in the two groups(12 positive schizophrenics, 7 negative schizophrenics) and $T_{30}$ levels were measured 30 minutes after intravenous injection of cimetidine (ie, 9:30 AM) Results: 1) Baseline prolactin levels were not different in the three groups. 2) Prolactin levels of 30 minutes after intravenous injection of cimetidine($T_{30}$) compared with baseline prolactin levels were increased all in the three groups. 3) Degrees of interval change from baseline to $T_{30}$ were significantly different between normal control and negative schizophrenics(p<0.05). Conclusion : The prolactin response to cimetidine was significantly blunted in negative male schizophrenics than normal control. These data are consistent with the hypothesis of an abnormality of serotonergic activity, including down-regulation $5-HT_2$ receptors, in male negative schizophrenics.

• Journal of Life Science
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• v.17 no.11
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• pp.1576-1581
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• 2007

Dopamine reward pathway projecting from ventral tegmental area to nucleus accumbens is well known as playing an important role in alcohol dependence. It is supposed that this dopamine pathway is modulated by $5-HT_3$ nervous system, and it was reported that ondansetron (OND), $5-HT_3$ receptor antagonist, reduced drinking amount and increased abstinence rate in alcohol-dependent patients. The purpose of this study is to investigate the effect of combination of OND and naltrexone (NTX), non-specific opioid receptor antagonist, on alcohol intake in C57BL/6 mice. In 40 C57BL/6 mice in the state of alcohol dependence, vehicle, while OND 0.01 mg/kg, or NTX 1.0 mg/kg administrated respectively, or OND 0.01 mg/kg and NTX 1.0 mg/kg administrated simultaneously for ten days, medication effects on 2-hr alcohol, 22-hr water, 24-hr food intake and body weight were studied. When vehicle group was compared with 3 medication groups respectively, using a repeated measure ANOVA, NTX alone and vehicle groups showed a significant medication by time interaction (p=0.042) in 2-hr alcohol intake, but in the other 2 groups, OND and NTX combination group and OND alone group, there was no significant interaction with vehicle group in 2-hr alcohol intake. From these results, it is suggested that there is no effect on alcohol intake in mice treating with OND, and naltrexone#s suppression effect on alcohol intake in mice is attenuated when treating with OND and NTX simultaneously. It is supposed that a further study looking at the interactions of serotonin, dopamine and opioid nerves systems will be needed.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.5
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• pp.285-289
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• 2010

In the present study, the antinociceptive profiles of $Campanula$ $punctata$ extract were examined in ICR mice. The $Campanula$ $punctata$ contain a large dose of saponin. $Campanula$ $punctata$ extract administered orally (200 mg/kg) showed an antinociceptive effect as measured by the tail-flick and hot-plate tests. In addition, $Campanula$ $punctata$ extract attenuated the writhing numbers in the acetic acid-induced writhing test. Furthermore, the cumulative nociceptive response time for intrathecal (i.t.) injection of substance P ($0.7{\mu}g$) was diminished by $Campanula$ $punctata$ extract. Intraperitoneal (i.p.) pretreatment with yohimbine (${\alpha}_2$-adrenergic receptor antagonist) attenuated antinociceptive effect induced by $Campanula$ $punctata$ extract in the writhing test. However, naloxone (opioid receptor antagonist) or methysergide (5-HT serotonergic receptor antagonist) did not affect antinociception induced by $Campanula$ $punctata$ extract in the writhing test. Our results suggest that $Campanula$ $punctata$ extract shows an antinociceptive property in various pain models. Furthermore, this antinociceptive effect of $Campanula$ $punctata$ extract may be mediated by ${\alpha}_2$-adrenergic receptor, but not opioidergic and serotonergic receptors.

• Bulletin of the Korean Chemical Society
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• v.27 no.8
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• pp.1189-1193
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• 2006

In order to develop radiopharmaceuticals for targeting a serotonin receptor such as $5-HT_{1A}$, histidine-$C_n$-arylpiperazines (AP) (C = alkyl, n = 2, 3, 4) were prepared in five steps with yields of 25%, 37% and 51%, respectively, and radiolabeled with the $[^{99m}Tc(CO)_3(H_2O)+3]^+$. The $^{99m}Tc(CO)_3$-Histidine-Cn-APs were prepared with a high yield (>99%) and characterized as a tridentate complex with a neutral charge to pass through the blood-brain barrier (BBB). The rhenium complexes with $Re(CO)_3$ were also synthesised and comparative experiments were achieved to evaluate the nature of the $^{99m}Tc$ complexes.

• CELLMED
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• v.13 no.14
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• pp.15.1-15.15
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• 2023

Background and objective: A new formular CPC22 consists of Cynanchum wilfordii root, Pueraria thomsonii flower, and Citrus unshiu peel and has been developed to improve the postmenopausal symptoms. The research intended to evaluate whether CPC22 would regulate bone loss, hot flashes, and dysregulated lipid metabolism in ovariectomized (OVX) postmenopausal mice. Method: The OVX mice were orally administered with CPC22 daily for 7 weeks. Results: CPC22 regulated OVX-induced bon loss by enhancing serum osteoprotegerin, alkaline phosphatase, and osteocalcin levels and diminishing serum receptor-activator of the NF-κB ligand (RANKL), collagen type 1 cross-linked N-telopeptide, and tartrate-resistant acid phosphatase levels. As a result of CPC22 treatment, notable decreases in tail skin temperature and rectal temperature were observed, along with diminishment in hypothalamic RANKL and monoamine oxidase A levels and enhancement in hypothalamic serotonin (5-HT), norepinephrine, dopamine, 5-HT2A, and estrogen receptor-β levels. CPC22 enhanced levels of serum estrogen and diminished levels of serum follicle-stimulating hormone and luteinizing hormone. CPC22 regulated levels of serum lipid metabolites, including total cholesterol, triglycerides, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol. Furthermore, CPC22 diminished levels of serum blood urea nitrogen, creatine kinase, alanine transaminase, aspartate aminotransferase, and lactate dehydrogenase and restored vaginal dryness without affecting uterus atrophy index and vagina weights. Conclusion: Therefore, these results indicated that CPC22 improves OVX-induced bone loss, hot flashes, and dysregulated lipid metabolism by compensating for estrogen deficiency without side effects, suggesting that CPC22 may be used for the prevention and treatment of post menopause.