• 한국식품영양학회지
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• 제18권4호
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• pp.295-301
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• 2005

Effects of leucocyanidins on the level of serum lipids and lipid peroxidation was investigated in 2,3,7,8-tetrachlorodibenzo-p-dioxine(TCDD)-induced rat that were pretreated with leucocyanidins for 4 weeks. The rats were divided into five experimental groups that is leucocyanidins and low TCDD treated group(LTL, 0.1 ${\mu}\;g/kg$ TCDD), leucocyanidins treated high TCDD group(LTH, 10 ${\mu}\;g/kg$ TCDD), No leucocyanidins and low TCDD treated group(NTL, 0.1 ${\mu}\;g/kg$ TCDD) and no leucocyanidins and high TCDD treated group(NTL, 10 ${\mu}\;g/kg$ TCDD). Serum total cholesterol, LDL-cholesterol and triglyceride level were significantly decreased and HDL-cholesterol level significantly increased in leucocyanidins treated group. Serum MDA level was also significantly reduced in leucocyanidins treated group. These results suggest that pre-supplement of leucocyanidins prevented the degree of lipid peroxidation on TCDD induced rat.

• The Korean Journal of Physiology and Pharmacology
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• 제5권2호
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• pp.177-181
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• 2001

Recently, nonsteroidal anti-inflammatory drugs (NSAIDs) have been found to be useful in the chemoprevention of colon cancer. To investigate whether indomethacin, an NSAIDs, induces apoptosis and thus assess the possibility of its application in the chemoprevention of human lung cancer, we have performed MTT assay, TUNEL assay, DAPI staining, and flow cytometric analysis using human lung carcinoma cell line NCI-H1299. Through morphological and biochemical analyses, it was demonstrated that NCI-H1299 cells treated with indomethacin (0.5 mM) exhibit classical apoptotic features. These results suggest that indomethacin induces apoptosis in NCI-H1299 cells and that NSAIDs, including indomethacin, may be a useful tool for the chemoprevention of human lung cancer.

• Journal of Ginseng Research
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• 제15권1호
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• pp.6-12
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• 1991

The analgesic effect of morphine was antagonized in mice pretreated with ginseng total saponin intraperitoneally, intracerebrally and intrathecally. The antagonized effects of morphine analgesia were reversed predominantly by treatment with L-3, 4-dihydroxyphenylalanine in the tail pinch test and 5-hydroxytryptophan in the tail flick test respectively. These indicate that the antagonistic action of ginseng total saponin might be due to their inhibitions of the activation of descending ihibitory systems at the cerebral site as well as spinal. In addition, any appreciable changes of brain biogenic monoamine levels were not observed in mice pretreated with ginseng total saponin at various time intervals. These results obtained suggest that a newly equilibrated state of neurologic function could be found in mice pretreated with ginseng total saponin, and modification of neurologic function in the mechanism for the antagonism of morphine analgesia by ginseng total saponin was more important than the changes of brain biogenic monoamine levels.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2002년도 Molecular and Cellular Response to Toxic Substances
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• pp.162-162
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• 2002

There has been many findings of natural, environmental or manufactered nonsteroidal substances shown to have estrogenic activity. Since estrogens affect reproduction and cellular development to cause disease in people or animals, chronic exposure may have a major impact on health.(omitted)

• The Korean Journal of Physiology and Pharmacology
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• 제17권5호
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• pp.469-477
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• 2013

This study investigated effect of extract containing quercetin-3-O-${\beta}$-D-glucuronopyranoside from Rumex Aquaticus Herba (ECQ) against chronic gastritis in rats. To produce chronic gastritis, the animals received a daily intra-gastric administration of 0.1 ml of 0.15% iodoacetamide (IA) solution for 7 days. Daily exposure of the gastric mucosa to IA induced both gastric lesions and significant reductions of body weight and food and water intake. These reductions recovered with treatment with ECQ for 7 days. ECQ significantly inhibited the elevation of the malondialdehyde levels and myeloperoxidase activity, which were used as indices of lipid peroxidation and neutrophil infiltration. ECQ recovered the level of glutathione, activity of superoxide dismutase (SOD), and expression of SOD-2. The increased levels of total NO concentration and iNOS expression in the IA-induced chronic gastritis were significantly reduced by treatment with ECQ. These results suggest that the ECQ has a therapeutic effect on chronic gastritis in rats by inhibitory actions on neutrophil infiltration, lipid peroxidation and various steps of reactive oxygen species (ROS) generation.

• The Korean Journal of Physiology and Pharmacology
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• 제9권5호
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• pp.283-289
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• 2005

Endothelium, particularly pulmonary endothelium, is predisposed to injury by reactive oxygen species (ROS) and their derivatives. Heme oxygenase (HO) has been demonstrated to provide cytoprotective effects in models of oxidant-induced cellular and tissue injuries. In the present study, we investigated the effects of YS 49 against oxidant [tert-butylhydroperoxide (TBH)]-induced injury using cultured sheep pulmonary artery endothelial cells (SPAECs). The viability of SPAECs was determined by quantifying reduction of a fluorogenic indicator Alamar blue. We found that TBH decreased cell viability in a timeand concentration-dependent manner. YS 49 concentration- and time-dependently increased HO-1 induction on SPAECs. As expected, YS 49 significantly decreased the TBH-induced cellular injury. In the presence of zinc protophorphyrin, HO-1 inhibitor, effect of YS 49 was significantly inhibited, indicating that HO-1 plays a protective role for YS 49. Furthermore, YS 49 showed free radical scavenging activity as evidenced by 1,1-diphenyl-2-picrylhydrazyl (DPPH) and inhibition of lipid peroxidation. However, YS 49 did not inhibit apoptosis induced by lipopolysaccharide (LPS) in SPAECs. Taken together, HO-1 induction along with strong antioxidant action of YS 49 may be responsible for inhibition of TBH-induced injury in SPAECs.

• The Korean Journal of Physiology and Pharmacology
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• 제15권4호
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• pp.211-216
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• 2011

Glioblastoma multiforme is one of the most common and aggressive tumors in central nervous system. It often possesses characteristic necrotic lesions with hemorrhages, which increase the chances of exposure to thrombin. Thrombin has been known as a regulator of MMP-9 expression and cancer cell migration. However, the effects of thrombin on glioma cells have not been clearly understood. In the present study, influences of thrombin on glioma cell migration were examined using Boyden chamber migration assay and thrombin-induced changes in MMP-9 expression were measured using zymography, semi-quantitative RT-PCR, and Western blotting. Furthermore, underlying signaling pathways by which thrombin induces MMP-9 expression were examined. Thrombin-induced migration and MMP-9 expression were significantly potentiated in the presence of wortmannin, a PI3K inhibitor, whereas MAPK inhibitors suppressed thrombin-induced migration and MMP-9 expression in C6 glioma cells. The present data strongly demonstrate that MAPK and PI3K pathways evidently regulate thrombin-induced migration and MMP-9 expression of C6 glioma cells. Therefore, the control of these pathways might be a beneficial therapeutic strategy for treatment of invasive glioblastoma multiforme.

• The Korean Journal of Physiology and Pharmacology
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• 제17권4호
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• pp.321-329
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• 2013

Rodents exposed to a 15-min pretest swim in the forced swimming test (FST) exhibit prolonged immobility in a subsequent 5-min test swim, and antidepressant treatment before the test swim reduces immobility. At present, neuronal circuits recruited by antidepressant before the test swim remain unclear, and also less is known about whether antidepressants with different mechanisms of action could influence neural circuits differentially. To reveal the neural circuits associated with antidepressant effect in the FST, we injected desipramine or citalopram 0.5 h, 19 h, and 23 h after the pretest swim and observed changes in c-Fos expression in rats before the test swim, namely 24 h after the pretest swim. Desipramine treatment alone in the absence of pretest swim was without effect, whereas citalopram treatment alone significantly increased the number of c-Fos-like immunoreactive cells in the central nucleus of the amygdala and bed nucleus of the stria terminalis, where this pattern of increase appears to be maintained after the pretest swim. Both desipramine and citalopram treatment after the pretest swim significantly increased the number of c-Fos-like immunoreactive cells in the ventral lateral septum and ventrolateral periaqueductal gray before the test swim. These results suggest that citalopram may affect c-Fos expression in the central nucleus of the amygdala and bed nucleus of the stria terminalis distinctively and raise the possibility that upregulation of c-Fos in the ventral lateral septum and ventrolateral periaqueductal gray before the test swim may be one of the probable common mechanisms underlying antidepressant effect in the FST.

• The Korean Journal of Physiology and Pharmacology
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• 제4권2호
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• pp.99-104
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• 2000

We investigated the action of NOS inhibitors on NOS in rats. Both of nitric oxide synthase inhibitors, $N^G$-monomethyl-L-arginine $(L-NMMA,\;3\;{\mu}M)$ or $N^G$-nitro-L-arginine methylester $(L-NAME,\;30\;{\mu}M),$ augmented phenylephrine $(PE,\;10^{-7}\;M)-induced$ contraction which was inhibited by acetylcholine (ACh) in rat thoracic aorta. This augmentation by L-NAME or L-NMMA was attenuated with the treatment of NO precursor, arginine. ACh, however, decreased the augmentation induced by L-NMMA, but not by L-NAME. Superoxide dismutase (SOD, 50 u/ml) potentiated an inhibitory effect of ACh on the PE $(10^{-7}\;M)-induced$ contraction. It has been known that platelet activating factor itself induces iNOS. Platelet activating factor $(PAF,\;10^{-7}\;M)$ inhibited PE $(10^{-7}\;M)-induced$ contraction. Pretreatment with L-NMMA (30 mM) or L-NAME (30 mM) significantly blocked the inhibitory action of PAF on PE-induced contraction. L-NMMA (100 mM) or L-NAME (100 mM) reduced nerve conduction velocity (NCV) relevant to nNOS in rat sciatic nerve. ACh attenuated the reduction of NCV by L-NMMA-, but not by L-NAME-induced reduction of NCV. These results suggest that L-NMMA and/or L-NAME have different action on three types of NOS in rats.

• The Korean Journal of Physiology and Pharmacology
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• 제12권3호
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• pp.117-123
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• 2008

Although growth associated protein-43 (GAP-43) is known to playa significant role in the regulation of axonal growth and the formation of new neuronal connections in the hippocampus, there is only a few studies on the effects of acute stress on GAP-43 mRNA expression in the hippocampus. Moreover, the effects of repeated citalopram treatment on chronic mild stress (CMS)-induced changes in GAP-43 mRNA expression in the hippocampus have not been explored before. To explore this question, male rats were exposed to acute immobilization stress or CMS. Also, citalopram was given prior to stress everyday during CMS procedures. Acute immobilization stress significantly increased GAP-43 mRNA expression in all subfields of the hippocampus, while CMS significantly decreased GAP-43 mRNA expression in the dentate granule cell layer (GCL). Repeated citalopram treatment decreased GAP-43 mRNA expression in the GCL compared with unstressed controls, but this decrease was not further potentiated by CMS exposure. Similar decreases in GAP-43 mRNA expression were observed in CA1, CA3 and CA4 areas of the hippocampus only after repeated citalopram treatment in CMS-exposed rats. This result indicates that GAP-43 mRNA expression in the hippocampus may differently respond to acute and chronic stress, and that repeated citalopram treatment does not change CMS-induced decreases in GAP-43 mRNA expression in the GCL.