• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1188-1198
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• 1998

Background : The purpose of the present study was to determine the protective effect of antiasthmatic activity of inhaled heparin, cromolyn sodium, budesonide, furosemide in exercise-induced asthma(EIA). The other important considerable point of this study was the mechanism of bronchoconstriction on EIA. Methods : Eight subjects with a history of EIA were studied on 5 different experiment days. After obtaining baseline $FEV_1$ and FVC, subjects performed a standardized exercise challenge. EIA was assessed by measurement of $FEV_1$ before and after exercise. On experiment day 4, the exercise challenge was performed after the subjects inhaled either heparin (1,000 units/kg/day for 5 days), furosemide (1mg/kg for 5 days), cromolyn (4mg/day for 5 days), or budesonide ($400{\mu}g/day$ for 5 days). On experiment day 5, the methacholine bronchial provocation test was performed. On experiment day 3, activated partial thromboplastine time(aPTI) was checked. Results : Maximum decrements of $FEV_1$ (mean${\pm}$SE) among 0 to 120 minutes after exercise were as follows : heparin was $83.1{\pm}4.81%$ (p=0.010), furosemide was $80.5{\pm}6.87%$ (p=0.071), cromolyn was $86.8{\pm}6.53%$ (p=0.340), and budesonide was $79.4{\pm}7.31%$ (p=0.095). Above medications were compared to the control value ($72.5{\pm}18.2%$) by paired t-test. No medications had effect on $PD_{20}$ of methacholine bronchial provocation test The results were control $1.58{\pm}0.49{\mu}mol$), heparin ($4.17{\pm}1.96{\mu}mol$), furosemide ($1.85{\pm}0.86{\mu}mol$), cromolyn ($2.19{\pm}0.89{\mu}mol$), and budesonide ($3.38{\pm}1.77{\mu}mol$), respectively(p>0.05). The inhaled heparin had no effect of anticoagulation. Conclusion : These data demonstrate that inhaled heparin has a protective effect on EIA. The effect of inhaled cromolyn was statistically absent with manufacture's recommended dosage on EIA. So, the dosage of cromolyn should be carefully evaluated in future. Although inhalation of budesonide and furosemide have no statistical significance compared to control, these drugs also have some protective effects on EIA.

• The Journal of Korean Obstetrics and Gynecology
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• v.30 no.2
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• pp.16-36
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• 2017

Objectives: The purpose of this study was to evaluate the anti-climacterium effects of Jibaekjihwang-tang (JBJHT), especially on estrogenic, anti-obesity, hypolipidemic, hepatoprotective against fatty liver and anti-osteoporotic effects by Ovariectomy (OVX) mice. Methods: In order to evaluate anti-climacterium effects of JBJHT, we used bilateral OVX female ddY mice. In this study, six groups were used; sham control, OVX control, estradiol, JBJHT 500, 250 and 125 mg/kg treated groups. Since 28 days after OVX surgery, JBJHT extracts were orally treated, and $17{\beta}$-estradiol $0.03{\mu}g/head$ were subcutaneously injected for 84 days, once a day. And then, we observed anti-climacterium effects classified into five categories; estrogenic, anti-obesity, hypolipidemic, hepatoprotective against fatty liver and anti-osteoporotic effects. The results were compared with $17{\beta}$-estradiol $0.03{\mu}g/head$/day subcutaneous treated OVX mice. Results: OVX control mice showed noticeable hypertrophic changes of adipocytes in abdominal fat pads, fatty liver, uterine atrophic changes, decreases of bone strength were also observed in OVX control. However, these estrogen-deficient climacterium symptoms were significantly and dose-dependently inhibited by JBJHT 500, 250 and 125 mg/kg treatment. Moreover, JBJHT 500 mg/kg showed comparable inhibitory effects as compared to those of estradiol $0.03{\mu}g/head$/day subcutaneous treatment. Conclusions: The results suggest that oral administration of JBJHT 500, 250 and 125 mg/kg has clear dose-dependent anti-climacterium effects in OVX mice.

• Journal of Life Science
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• v.23 no.3
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• pp.462-469
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• 2013

Withaferin A is a steroidal lactone purified from the Indian medicinal plant Withania somnifera. It exhibits a wide variety of activities, including anti-tumor, anti-inflammation, and immunomodulation properties. In this review, we focused on the anti-cancer effects of withaferin A. Withaferin A inhibits cell proliferation, metastasis, invasion, and angiogenesis in cancer cells. Furthermore, it sensitized irradiation, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-, and doxorubicin-mediated apoptosis. The results showed that multiple mechanisms were involved in withaferin A-mediated anti-cancer effects. First, withaferin A increased intracellular reactive oxygen species (ROS) production and induced ER stress- and mitochondria-mediated apoptosis. Second, withaferin A inhibited the signaling pathways (Jak/STAT, Akt, Notch, and c-Met), which are important in cell survival, proliferation, and metastasis. Third, it induced apoptosis and inhibited cancer cell migration through the up-regulation of prostate apoptosis protein-4 (Par-4). Finally, withaferin A up-regulated pro-apoptotic protein expression levels through the inhibition of proteasome activity. Our findings suggested that withaferin A is a potential, potent therapeutic agent.

• Korean journal of applied entomology
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• v.50 no.3
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• pp.227-233
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• 2011

Crysochroa fulgidissima (Bidan-beole, Spanish fly) is traditionally used as a crude drug and insecticide in the East Asia and Korea, respectively. This study investigated the effect of ethanol extract of C. fulgidissima on the NO production activity. The C. fulgidissima extract was a potent inducer of NO production in CPAE cells and a stimulator of endothelial nitric oxide synthase in a dose-dependent manner. This study also evaluated the anti-inflammatory activity of this extract by determining the level of ICAM-1, VCAM-1, and prostaglandin $E_2$ from HUVEC cells. Although C. fulgidissima extract was a potent inducer of NO production in the CPAE cells, it showed weak inhibitory effects on vascular endothelial growth factor (VEGF) production in HUVEC cells. HPLC and GC-MS analysis of the ethanol extract of C. fulgidissima revealed the presence of cantharidin.

• The Korean Journal of Pharmacology
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• v.20 no.2
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• pp.7-14
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• 1984

In pithed rats, rising in diastolic blood pressure by clonidine, when intravenously injected, is expressed as the postsynaptic action, and inhibitory action on electrical stimulation-induced tachycardia by clonidine is expressed as the presynaptic inhibitory action. In this study it was aimed to observe the inhibitory effect of imipramine caused by a single and chronic administration on both postsynaptic and presynaptic action of clonidine in pithed rats, and discussed in relation with the mechanism of antidepressant action of imipramine. 1) A rise of diastolic blood pressure by clonidine was not antagonized by prazosin, but by both phentolamine and piperoxan. 2) The inhibition by clonidine of tachycardia which was induced by electrical stimulation was also antagonized by phentolamine and piperoxan, but not by prazosin. 3) The increase in diastolic blood pressure in response to clonidine was inhibited by both a single or chronic administration with imipramine (20 mg/kg). It was more pronounced in the latter. 4) The inhibitory action of clonidine on the tachycardia was markedly inhibited by both types of administration with imipramine, between which there showed little difference. It is concluded that the presynaptic ${\alpha}_2-adrenoceptor$ is rather sensitively affected by a single administration with imipramine, and a long-term imipramine treatment may inhibit both pre- and postsynaptic ${\alpha}_2-adrenoceptors$, simultaneously. Furthermore, it was seemed unlikely that these results provide the evidence :to support the fact that the subsensitivity of presynaptic ${\alpha}_2-adrenoceptor$ may be the mechanism of action of tricyclic antidepressant.

• Tuberculosis and Respiratory Diseases
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• v.39 no.1
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• pp.42-54
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• 1992

Background:It has been suggested that the cyclooxygenase metabolites play an important role in changes of early hemodynamic parameters in the endotoxin-induced acute lung injury. But there have been many debates about their role in the late increase of alveolar-capillary permeability, and it is not known whether they act directly or indirectly through oxygen free radicals which have been known to be produced during the metabolic process of cyclooxygenase pathway. So we performed this study to identify the pathogenetic role of cyclooxygenase metabolites in the endotoxin-induced acute lung injury in domestic pigs. Method: We infused endotoxin into 8 domestic pigs; endotoxin only (n=3), and pretreatment with indomethacin (n=5). We observed the sequential changes in hemodynamic parameters, the concentration of plasma oxidized glutathione (GSSG) in pulmonary arterial and venous blood, and albumin content in bronchoalveolar lavage fluid (BALF). Results: 1) While cardiac output decreased, mean pulmonary arterial pressure, pulmonary vascular resistance, and alveolar-arterial oxygen difference increased over phase 1 (0-2hr) and phase 2 (2-4.5hr) by endotoxin, indomethacin attenuated the decrease in cardiac output during phase 1 and increase in mean pulmonary arterial pressure, pulmonary vascular resistance, and alveolar-arterial oxygen difference during both phases. 2) The increase in plasma GSSG content during phase 2 was not attenuated by indomethacin. 3) The content of BALF albumin was significantly lower in indomethacin groups than that of endotoxin group. Conclusion: These results suggest that it is likely that cyclooxygenase metabolites have an effect on endotoxin-induced acute lung injury during both phases probably through direct action.

• Applied Biological Chemistry
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• v.44 no.3
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• pp.148-152
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• 2001

This study investigated the role of excitatory amino acid systems in the initiation of organophosphate-induced seizures and brain damages in rats through quantitative in vivo microdialysis. Microdialysates were collected from the hippocampus of rat brain, treated with diisopropylfluorophosphate (DFP; 2.67 mg/kg, s.c.) alone, and/or atropine sulfate (15 mg/kg, i.m.) and procyclidine (30 mg/kg, i.m.). The protective effects of atropine, a muscarinic blocker, and/or procyclidine, a N-methyl-D-aspartate and cholinergic antagonist, against DFP were examined. DFP treatment increased the levels of aspartate (Asp) and glutamate (Glu) significantly in the hippocampal persuate with the induction of seizures. Treatment of procyclidine could effectively block the increase of Asp and Glu levels. Atropine treatment showed no significant anticonvulsive effects against DFP-induced seizures. The increases of Asp and Glu levels by DFP were also completely blocked through the combined treatment of atropine and procyclidine. Histopathological findings on the hippocampus confirmed the above results. More effective protection was observed through the treatments of procyclidine alone or of both procyclidine and atropine than atropine alone against DFP-induced brain damage. Procyclidine was shown to be effective in DFP-induced seizures.

• The Korean Journal of Pharmacology
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• v.24 no.2
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• pp.165-178
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• 1988

In this study, the effect of single or repeated (daily for 7 or 14 days) electroconvulsive shock (ECS) on central and peripheral opiate system and modification of the actions of ECS by several psychoactive drugs were investigated in the rat. Repeated ECS caused increase of Met-enkephalin content and decrease of Bmax of specific $[^3H]$imorphine binding in the rat brain. These effects were persisted more than 7 days after the last ECS, but single ECS failed to show these effects. However, ${\beta}-endorphin$ content was decreased in midbrain preparation and increased in plasma by repeated or single ECS. These phenomenon was seen shortly after the last ECS. After ECS-induced seizure was prevented by phenobarbital, ECS-induced increase in Met-enkephalin content was significantly attenuated. Imipramine or pargyline did not affect the action of repeated ECS. On the other hand, reserpine, chlorpromazine or haloperidol which were classified as neuroleptic antipsychotics, augmented the ECS-induced changes of central and peripheral opiate parameters. Furthermore, in groups received repeated ECS, changes of Bmax of specific $[^3H]-morphine binding$ binding was inversely correlated with changes of Met-enkephalin contents, but not with changes of ${\beta}-endorphin$ contents. From these results, it is inferred that the central or peripheral opioidergic system may be involved in the therapeutic and/or adverse effects of ECS which also can be influenced by some psychoactive drugs.

• Nuclear Medicine and Molecular Imaging
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• v.40 no.6
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• pp.302-308
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• 2006

Purpose: Although several neuroanatomical models of panic disorder have been proposed, little is known regarding the neurological mechanisms underlying cognitive-behavioral therapy (CBT) in patients with panic disorder. This study was performed to identify the brain structures that show changes of regnioal cerebral blood flow (rCBF) after CBT in patients with panic disorder. Materials and Methods: Seven patients who were diagnosed as panic disorder by DSM-IV were treated with CBT for 8 weeks and twelve healthy volunteers joined in this study. Serial $^{99m}Tc-ECD$ brain perfusion SPECT images were acquisited and PDSS-SR (Self-Report version of Panic Disorder Severity Scale) and ACQ (Agoraphobic Cognitive Question) scores were measured just before and after CBT in all patients. Data were analyzed using SPM2. Results: Subjective symptoms were improved, and PDSS-SR and ACQ scores were significantly reduced ($14.9{\pm}3.9\;vs.\;7.0{\pm}1.8$, p<0.05; $30.3{\pm}8.5\;vs.\;21.6{\pm}3.4$, p<0.05, respectively) after CBT in panic patients. Before CBT, a significant increase of rCBF was found in the cingulate gylus, thalamus, midbrain, both medial frontal and temporal lobes of the panic patients compared to the normal volunteers. After CBT, we observed a significant rCBF decrease in the left parahippocamus, right insula and cingulate gyrus, both frontal and temporal lobes, and a significant rCBF increase in both the occipital lobes, left insula, both frontal and left parietal lobes. Conclusion: These data suggested that CBT is effective for panic disorder and diminish the activity of the brain areas associated with fear in panic disorder.

• Korean Journal of Food Science and Technology
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• v.35 no.1
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• pp.138-143
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• 2003

Total methanolic extract of Chrysanthemum coronarium L. var. spatiosum (Compositae) was revealed to have anti-hepatotoxic activity against galactosamine-induced toxicity on primary cultured rat hepatocytes. After successive partitioning with chloroform, n-butanol, and water, the chloroform fraction showed a significant inhibition activity of 51% at 50 ppm, compared with that of silybin, 45.9% at $100\;{\mu}M$. The chloroform fraction was subjected to silica gel column chromatography and yielded active CH-II, CH-V and CH-VI subfractions, and the anti-hepatotoxic activity of these subfractions were 47.6, 56.3, and 23.2%, respectively, at 50 ppm. Total glutathione contents of CH-II, CH-V, and CH-VI increased by 49.8, 43.9, and 47.5% of the control, respectively at 50 ppm, whereas that of silymarin was, 59.7% at $100\;{\mu}M$ after challenged with galactosamine. The ratio of (reduced glutathione) / (total glutathione) in CH-II, CH-V and CH-VI subfraction showed similar values of $0.86{\sim}0.87$ at 50 ppm, whereas that of silymarin was, 0.85 at $100\;{\mu}M$. The incorporation of $[^3H]-uridine$ uptake into RNA was not affected by these active subfractions.