• Journal of Nutrition and Health
• /
• v.35 no.2
• /
• pp.171-182
• /
• 2002

This study wa performed to investigate the effect of dired powder of chestnut and acorn on lipid metabolism, antioxidative capacity and antithrombotic effect in rats. Fifty-four male Sprague-Dawley rats weighing 199$\pm$17g were blocked into nine groups according to their body weight. Rats were raised with diets containing only flesh or flesh with inner skin of 5% and 10% dried nut powders for four weeks. Food intake, body weight gain, food efficiency ratio and organ weight were no different among the experimental groups. The plasma and liver lipid levels of all the nut diet groups were lover than those of the control group. The nut diets showed hypolipidenic effect in the plasma and liver. Plasma and liver thiobarbituric acid reactive substance (TBARS) concentrations were significantly decreased in all the nut diet groups. The plasma TBARS levels of the inner skin groups were significantly different from the control group dose-dependently. Superoxide dismutase(SOD) activity was significantly different among the experimental groups, and all the nut groups showed higher activity than the control group. There were significant differences in SOD activity between the chestnut and acorn groups and the chestnut groups showed higher erythrocyte SOD activity and the acorn groups showed higher liver SOD activity than the other groups. Whereas catalase and GSH-Px activities in the erythrocyte and liver of both nut groups showed a tendency to increase, they were not significantly different among the experimental groups. The bleeding time and whole blood clotting time tended to be extended by feeding both types of nut but they were not significantly different among the experimental groups. Production of TX $B_2$ and PG $F_{1{\alpha}}$ was no different among the experimental groups. These results suggest that chestnut and acorn diets have the effect of lowering plasma and liver lipid levels, inhibiting lipid peroxide formation and increasing antioxidative enzymes activity. Thus, it is plausible that chestnut and acorn could be recommended in the treatment and prevention of cardiovascular diseases.

• Development and Reproduction
• /
• v.4 no.2
• /
• pp.243-250
• /
• 2000

To find the mechanism underlying the ADP-induced increase in the outward current in ovulated mouse oocytes, we examined changes in voltage-dependent currents using the whole cell voltage clamp technique and the internal perfusion technique. Eggs were collected from the oviduct of superovulated mice with PMSG and hCG. Membrane potential was held at -60 mV (or -80 mV in the case of recording $Ca^{2＋}$ currents) and step depolarizations or hyperpolarizations were applied for 300 ms. By step depolarizations, outward currents comprising steady-state and time-dependent components were elicited. They were generated in response to the positive potential more than 20 mV with severe outward rectification and were blocked by external TEA, a specific $K^{＋}$ channel blocker, suggesting that they be carried via $K^{＋}$ channels. Internally-perused 5 mM ADP gradually increased outward $K^{＋}$ currents (IK) 1 min after perfusion of ADP and reached slowly to maximum (150~170％) 5 min later over the positive potential range, implying that ADP might not be acted directly to the $K^{＋}$ channels. IK were decreased by 5 mM ATP without affecting the steady-state component of outward current. In contrast to the effect of ADP and ATP on IK, both effect of ATP and ADP on inward $Ca^{2＋}$ currents (ICa) could not be detected due to the continuous decrease in current amplitudes with time-lapse ("run-down" phenomena). To check if there is a G protein-involved regulation in the ionic current of mouse oocytes, 1 mM GTP was applied to the cytoplasmic side, and the outward current and inward currents were recorded. ICa was promptly increased in the presence of GTP whereas IK was not changed. from these results, it is concluded that the ATP-dependent regulation is likely linked in the ADP-induced increase in the outward $K^{＋}$ current, and G protein-involved cellular signalling might affect ion channels carrying $Ca^{2＋}$ and $K^{＋}$ in mouse oocytes.

• The Korean Journal of Pharmacology
• /
• v.18 no.1
• /
• pp.17-22
• /
• 1982

Zizyphus seed(Zizyphus vulgaris Lamark var. Spinosus Bunge) has long been used as hypnotics and sedatives in oriental medicine, and it is reported that the Zizyphus seed elicited a variety of pharmacologic actions besides CNS depression. Present study was undertaken to investigate the effects of Zizyphus seed on the central nervous system and on the blood pressure. The effect of Zizyphus seed on the central nervous system was measured by the influence of thiopental sleeping time and by inhibition of chemical convulsion (strychnine and pentylenetetrazol induced). Blood pressure changes by Zizyphus extract and its mode of action were investigated. The ground Zizyphus seed was extracted with hexane and methanol, consecutively and the supernatants were discarded. The precipitate was re-extracted with distilled water and the supernatant was evaporated to a dark-brownish sticky liquid, which was used as Zizyphus seed extract in this study after dissolving in saline prior to experiment. The results are as follows. 1) Zizyphus seed extract caused marked prolongation of the thiopental sleeping time in mice. 2) The chemical convulsion by strychnine and pentylenetetrazol, and the mortality by them in chicks were not affected by pretreatment of Zizyphus seed extract. 3) Zizyphus seed extract produced transient fall of blood pressure in the cat, and this hypotentive effect was blocked partially by atropine but not affected by bilateral vagotomy and/or hexamethonium, nor propranolol and, chlorpheniramine and/or cimetidine. With the above results, it may be suggested that the water extract of Zizyphus seeds contains components producing CNS depression and hypotension. Furthermore it is felt that the cholinergic effect, but not the adrenergic or histaminergic, is partly responsible for the hypotensive effect of Zizyphus seed extract.

• The Korean Journal of Physiology and Pharmacology
• /
• v.9 no.5
• /
• pp.255-262
• /
• 2005

Striatum is involved in the control of movement and habitual memory. It receives glutamatergic input from wide area of the cerebral cortex as well as an extensive serotonergic (5-hydroxytryptamine, 5-HT) input from the raphe nuclei. In our study, the effects of 5-HT on synaptic transmission were studied in the rat corticostriatal brain slice using in vitro whole-cell recording technique. 5-HT inhibited the amplitude as well as frequency of spontaneous excitatory postsynaptic currents (sEPSC) significantly, and neither ${\gamma}-aminobutyric$ acid (GABA)A receptor antagonist bicuculline (BIC), nor $N-methyl-_{D}-aspartate$ (NMDA) receptor antagonist, $_{DL}-2-amino-5-phosphonovaleric$ acid (AP-V) could block the effect of 5-HT. In the presence non-NMDA receptor antagonist, 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenxo[f] quinoxaline-7-sulfonamide (NBQX), the inhibitory effect of 5-HT was blocked. We also figured out that 5-HT change the channel kinetics of the sEPSC. There was a significant increase in the rise time during the 5-HT application. Our results suggest that 5-HT has an effect on both pre- and postsynaptic site with decreasing neurotransmitter release probability of glutamate and decreasing the sensitivity to glutamate by increasing the rise time of non-NMDA receptor mediated synaptic transmission in the corticostriatal synapses.

• The Korean Journal of Physiology and Pharmacology
• /
• v.17 no.1
• /
• pp.37-42
• /
• 2013

Taxifolin glycoside is a new drug candidate for the treatment of atopic dermatitis (AD). Many drugs cause side effects such as long QT syndrome by blocking the human ether-a-go-go related gene (hERG) $K^+$ channels. To determine whether taxifolin glycoside would block hERG $K^+$ channels, we recorded hERG $K^+$ currents using a whole-cell patch clamp technique. We found that taxifolin glycoside directly blocked hERG $K^+$ current in a concentration-dependent manner ($EC_{50}=9.6{\pm}0.7{\mu}M$). The activation curve of hERG $K^+$ channels was negatively shifted by taxifolin glycoside. In addition, taxifolin glycoside accelerated the activation time constant and reduced the onset of the inactivation time constant. These results suggest that taxifolin glycoside blocks hERG $K^+$ channels that function by facilitating activation and inactivation process.

• The Korean Journal of Physiology and Pharmacology
• /
• v.21 no.1
• /
• pp.125-131
• /
• 2017

Status epilepticus is the most common serious neurological condition triggered by abnormal electrical activity, leading to severe and widespread cell loss in the brain. Lithium has been one of the main drugs used for the treatment of bipolar disorder for decades, and its anticonvulsant and neuroprotective properties have been described in several neurological disease models. However, the therapeutic mechanisms underlying lithium's actions remain poorly understood. The muscarinic receptor agonist pilocarpine is used to induce status epilepticus, which is followed by hippocampal damage. The present study was designed to investigate the effects of lithium post-treatment on seizure susceptibility and hippocampal neuropathological changes following pilocarpine-induced status epilepticus. Status epilepticus was induced by administration of pilocarpine hydrochloride (320 mg/kg, i.p.) in C57BL/6 mice at 8 weeks of age. Lithium (80 mg/kg, i.p.) was administered 15 minutes after the pilocarpine injection. After the lithium injection, status epilepticus onset time and mortality were recorded. Lithium significantly delayed the onset time of status epilepticus and reduced mortality compared to the vehicle-treated group. Moreover, lithium effectively blocked pilocarpine-induced neuronal death in the hippocampus as estimated by cresyl violet and Fluoro-Jade B staining. However, lithium did not reduce glial activation following pilocarpine-induced status epilepticus. These results suggest that lithium has a neuroprotective effect and would be useful in the treatment of neurological disorders, in particular status epilepticus.

• Advances in Traditional Medicine
• /
• v.10 no.4
• /
• pp.254-262
• /
• 2010

Artemisia capillaris (A. capillaries) is known to play roles in many cellular events, such as cell proliferation, differentiation, and apoptosis. We investigated the antifibrogenic efficacy of A. capillaris in the immortalized human hepatic stellate cell line LX2. Cell proliferation was determined by the MTT assay. Cell cycle was analyzed by the flow cytometry. Apoptotic cells were measured using a cell death detection ELISA. Caspase activity was detected by a colorimetric assay. The mRNA level of Bcl-2 and Bax mRNA were measured by real-time PCR. MEK and ERK protein were detected by Western blot analysis. We provide evidence that A. capillaris induces cell cycle arrest, apoptosis, and potently inhibits the mitogen-activated protein kinase pathway. A. capillaris inhibited cell proliferation of LX2 cells in a dose- and time-dependent manner, increased the apoptosis fraction at cell cycle analysis with an accompanying DNA fragmentation, and resulted in a significant decrease in Bcl-2 mRNA levels and an increase in Bax expression. Exposure of LX2 cells to A. capillaris induced caspase-3 activation, but co-treatment of A. capillaris with the pan-caspase inhibitor Z-VAD-FMK, and the caspase-3 inhibitor Z-DEVE-FMK, blocked apoptosis. A. capillaris down-regulated Mcl-1 protein levels and inhibited phosphorylation of MEK/ERK, suggesting that it mediates cell death in LX2 cells through the down-regulation of Mcl-1 protein via a MEK/ERK-independent pathway.

• International Journal of Oral Biology
• /
• v.35 no.2
• /
• pp.69-74
• /
• 2010

The mu opioid receptor (MOR) has been regarded as the main site of interaction with analgesics in major clinical use, particularly morphine. The repressor element-1 silencing transcription factor (REST) functions as a transcriptional repressor of neuronal genes in non-neuronal cells. However, it is expressed in certain mature neurons, suggesting that it may have complex and novel roles. In addition, the interactions between MOR and REST and their functions remain unclear. In this study, we examined the effects of morphine on the expression of REST mRNA and protein in human neuroblastoma NMB cells to investigate the roles of REST induced by MOR activation in neuronal cells. To determine the effects of morphine on REST expression, we performed RT-PCR, real-time quantitative RT-PCR, western blot analysis and radioligand binding assays in NMB cells. By RTPCR and real-time quantitative RT-PCR, the expression of REST was found to be unchanged by either the MOR agonist morphine or the MOR specific antagonist CTOP. By western blot, morphine was shown to significantly inhibit the expression of REST, but this suppression was completely blocked by treatment with CTOP. In the radioligand binding assay, the overexpression of REST led to an increased opioid ligand binding activity of endogenous MOR in the NMB cells. These results together suggest that morphine inhibits the expression of REST in human neuroblastoma cells through a post-transcriptional regulatory mechanism mediated through MOR.

• Journal of the Korean Institute of Telematics and Electronics C
• /
• v.34C no.11
• /
• pp.1-11
• /
• 1997

The transient current components of the dRAM are analyzed and the sensing current, data path operation current and DC leakage current are revealed to be the major curretn components. It is expected that the supply voltage of less than 1.5V with low VT MOS witll be used in multi-giga bit dRAM. A low voltage dual VT self-timed CMOS logic in which the subthreshold leakage current path is blocked by a large high-VT MOS is proposed. An active signal at each node of the nature speeds up the signal propagation and enables the synchronous DRAM to adopt a fast pipelining scheme. The sensing current can be reduced by adopting 8 bit prefetch scheme with 1.2V VDD. Although the total cycle time for the sequential 8 bit read is the same as that of the 3.3V conventional DRAM, the sensing current is loered to 0.7mA or less than 2.3% of the current of 3.3V conventional DRAM. 4 stage pipeline scheme is used to rduce the power consumption in the 4 giga bit DRAM data path of which length and RC delay amount to 3 cm and 23.3ns, respectively. A simple wave pipeline scheme is used in the data path where 4 sequential data pulses of 5 ns width are concurrently transferred. With the reduction of the supply voltage from 3.3V to 1.2V, the operation current is lowered from 22mA to 2.5mA while the operation speed is enhanced more than 4 times with 6 ns cycle time.

• Molecules and Cells
• /
• v.27 no.3
• /
• pp.383-390
• /
• 2009

To investigate the regulatory mechanism underlying the contractile response in the intestinal smooth muscle of the nile tilapia (Orechromis niloticus), we used pharmacologic and molecular approaches to identify the muscarinic subreceptors and the intracellular signaling pathways involved in this motility. Myography assays revealed that an M1- and M3-subtype selective antagonist, but not a M2-subtype selective antagonist, inhibited carbachol HCl (CCH)-induced intestinal smooth muscle contraction. In addition, a phospholipase C inhibitor, but not an adenylate cyclase inhibitor, blocked the contractile response to CCH. We also cloned five muscarinic genes (OnM2A, OnM2B, OnM3, OnM5A, and OnM5B) from the nile tilapia. In the phylogenetic analysis and sequence comparison to compare our putative gene products (OnMs) with the sequences obtained from the near complete teleost genomes, we unexpectedly found that the teleost fish have respectively two paralogous genes corresponding to each muscarinic subreceptor, and other teleost fish, except zebrafish, do not possess muscarinic subreceptor M1. In addition, the expression pattern of the nile tilapia muscarinic subreceptor transcripts during CCH-induced intestinal smooth muscle contraction in the proximal intestinal tissue was analyzed by real-time PCR surveys and it was demonstrated that CCH increased the OnMs mRNA expression rapidly and transiently.