• The Korean Journal of Physiology
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• v.23 no.1
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• pp.119-127
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• 1989

This study was undertaken to investigate the effect of medial amygdala on the gastric acid secretion and plasma gastrin concentration in the rats with chronic gastric fistula. After the medial nucleus of amygdala was damaged bilaterally by radiofrequency a. c. through stereotaxically inserted electrodes, the gastric juice was collected in the basal and histamine-stimulated states for 1 hour. The gastric juice was also collected while the medial nucleus of amygdala was stimulated with biphasic square wave in the both states. After the collection of the gastric juice, blood samples were drawn from the abdominal aorta for the radioimmunoassay of plasma gastrin. The results were as follows: 1) The damage of the medial amygdala significantly decreased the gastric juice volume and the acid output in the histamine-stimulated state. 2) The electrical stimulation of the medial amygdala significantly increased the gastric juice volume and the acid output in the histamine-stimulated state, and the acid output in the basal state. 3) The damage of the medial amygdala significantly decreased the plasma gastrin concentration but the electrical stimulation of the medial amygdala did not affect the plasma gastrin concentration. It is therefore suggested that the medial amygdala has a facilitatory influence on the histamine-stimulated gastric acid secretion in rats, and the influence may not be attributed to gastrin release.

• Mycobiology
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• v.33 no.1
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• pp.23-29
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• 2005

The effects of different concentrations of three amino acids as carbon and or nitrogen sources on mycelial dry weights, changes in pH values of synthetic medium, ammonia secretion and extracellular protease activity by three zoosporic fungi, pathogens of fish and shellfish, were studied. As compared with the control, the addition of isoleucine and aspartic acid as nitrogen sources were generally stimulative for mycelial dry weight production whereas phenylalanine was inhibitory irrespective to the tested fungal species. When amino acids served as carbon and nitrogen sources, the mycelial dry weights of the three fungi were increased (mostly non-significantly) relative to untreated control but weights were decreased as the concentrations of the three amino acids raised. The addition of individual amino acids as carbon and nitrogen sources to the medium significantly increased pH values of the medium comparable to the control. The addition of each of the three amino acids as carbon and nitrogen sources to the medium significantly induced ammonia secretion by the three species of zoosporic fungi. Ammonia secretion in synthetic medium amended with amino acids as nitrogen source raised by the three zoosporic fungi relative to untreated control except in case of Achlya racemosa treated with isoleucine. Extracellular protease activity was almost promoted in case of Achlya proliferoides and Saprolegnia furcata cultures treated with isoleucine and aspartic acid individually in presence of glucose and vice versa in case of phenylalanine. However, extracellular protease activity of A. racemosa decreased compared with the control at various concentrations of isoleucine and both phenylalanine and aspartic acid assumed inconsistent effects. Extracellular protease activity of the three zoosporic fungi in the medium devoid of glucose varied depending upon zoosporic fungal species, the tested amino acid and the applied concentrations. The values of protease activity were approximately less two folds than that obtained in presence of glucose.

• Preventive Nutrition and Food Science
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• v.8 no.3
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• pp.253-259
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• 2003

Conjugated linoleic acid (CLA) is a class of positional, geometric conjugated dienoic isomers of linoleic acid (LA). CLA activates the immune system, protects against tumorigenesis, and reduces the incidence of atherosclerosis. Trans-10, cis-12 CLA has specific effects on lipid metabolism, it has been shown to reduce body fat gain and regulates some adipocyte secreted proteins in vivo and in vitro. Here we report that a CLA mixture affects cytokine secretion from rat primary adipocytes. Rat primary adipocytes were treated with 1 mM, 100 $\mu$M, 1 $\mu$M or 100 nM CLA mixture doses; and leptin, tumor necrosis factor alpha (TNF a ), interleukin-6 (IL-6) and glycerol levels in the medium were measured. Leptin secretion was lower, TNF $\alpha$ secretion higher and IL-6 secretion did not change in response to the CLA mixture. Leptin and TNF $\alpha$ secretions did not change with CLA mixture treatment in a dose-dependent manner. In addition, the CLA mixture did not appear to enhance lipolysis in rat primary adipocytes. In conclusion, our study demonstrates that the decrease in leptin and increase in TNF $\alpha$ secretion in adipocytes treated with CLA mixture may be due to the apoptotic effect and to a reduction in peroxisome proliferator-activated receptor gamma (PPAR ${\gamma}$ ) ligands.

• The Korean Journal of Physiology
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• v.16 no.2
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• pp.177-186
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• 1982

The effect of ethacrynic acid (EA) on the renal secretion of PAH was examined in cat kidney. $C_{PAH}$ and $T_{PAH}$ were measured before and after infusion of EA $(0.5{\sim}50mg/kg)$ through the femoral vein. The following results were obtained: 1) In the dosage range of 0.5 to 25 mg/kg, EA increased the urine flow, and sodium and potassium excretion in dose-dependent manner, but the glomelular filtration rate was decreased as the dosage of EA was increased. 2) $C_{PAH}$ and $T_{PAH}$ were decreased by EA in the dosage range of 3 to 25 mg/kg and 1 to 50 mg/kg, respectively, in dose·dependent manner with the dosage to cause 50% inhibition of about 5 mg/kg. 3) With dosage of 0.5mg/kg, EA appeared to exert a great effect on diuretic response without the influence on $T_{PAH}$. At 10min after infusion of EA, a potent diuretic effect appeared, while $T_{PAH}$ did not show a significant change. These results suggest that the action mechanism of EA on tubular secretion of PAH may be different from that on natriuresis. 4) With dosage of 5 mg/kg, EA did not inhibit the Na-K-ATPase activity in microsomal fractions from both cortex and medulla. 5) The double reciprocal plot ($l/T_{PAH}$ versus $l/P_{PAH}$) suggested that EA inhibited the P AH secretion by a competitive pattern. However, probenecid, a prototypic inhibitor of the organic acid pump, had no influence on both the inhibitory effect of $T_{PAH}$ and the natriuretic effect by EA. These results suggest that in vivo EA altered tubular secretion of P AH through interactions with receptors that are not identical with the Na-K-ATPase.

• BMB Reports
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• v.54 no.5
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• pp.278-283
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• 2021

Our understanding of the differential effects between specific omega-3 fatty acids is incomplete. Here, we aimed to evaluate the effects of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) on T-helper type 1 (Th1) cell responses and identify the pathways associated with these responses. Naïve CD4⁺ T cells were co-cultured with bone marrow-derived dendritic cells (DCs) in the presence or absence of palmitate (PA), DHA, or EPA. DHA or EPA treatment lowered the number of differentiated IFN-γ-positive cells and inhibited the secretion of IFN-γ, whereas only DHA increased IL-2 and reduced TNF-α secretion. There was reduced expression of MHC II on DCs after DHA or EPA treatment. In the DC-independent model, DHA and EPA reduced Th1 cell differentiation and lowered the cell number. DHA and EPA markedly inhibited IFN-γ secretion, while only EPA reduced TNF-α secretion. Microarray analysis identified pathways involved in inflammation, immunity, metabolism, and cell proliferation. Moreover, DHA and EPA inhibited Th1 cells through the regulation of diverse pathways and genes, including Igf1 and Cpt1a. Our results showed that DHA and EPA had largely comparable inhibitory effects on Th1 cell differentiation. However, each of the fatty acids also had distinct effects on specific cytokine secretion, particularly according to the presence of DCs.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.4
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• pp.315-321
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• 2001

This study was aimed to evaluate the effects of quercetin and desferrioxamine on the development of the reflux esophagitis induced surgically, on gastric secretion and on lipid peroxidation which is a marker of oxidative stress. Omeprazole was used as a positive control drug. Omeprazole significantly and dose-dependently prevented the development of reflux esophagitis, but quercetin or desferrioxamine prevented only at high dose. Omeprazole significantly and dose-dependently inhibited the gastric acid secretion (gastric volume, pH and acid output), but quercetin or desferrioxamine did not inhibit. Malonyldialdehyde content, the end product of lipid peroxidation, increased significantly after the induction of reflux esophagitis. Omeprazole prevented lipid peroxidation. Quercetin and desferrioxamine inhibited the lipid peroxidation independent of their actions on gastric secretion. This result indicates that omeprazole confirmed preventing effect of rat reflux esophagitis, but quercetin and desferrioxamine inhibited esophagitis by reduction of lipid peroxidation irrespective of gastric acid secretion.

• YAKHAK HOEJI
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• v.36 no.2
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• pp.173-179
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• 1992

The rhizoma of Zingiber officinale has been used as antiemetic, expectorants, stomachache relieving drugs and digestive accelerators. From the observation of antigastritic action of the methanol extract of the rhizoma, it was fractionated with hexane, chloroform, ethyl acetate and butanol, followed by bioassay on antigastritic and antiulcerative activity. The hexane and the chloroform fraction reduced significantly HCl ethanol induced gastric lesion at the dose of 370 and 210 mg/kg, p.o., respectively. On the gastric ulceration and gastric secretion in pylorus-ligated rats, the hexane fraction decreased the volume of gastric secretion and acid output, and also increased pH at the dose of 370 mg/kg, i.d.. It showed considerable curative ratio of acetic acid induced ulcer without inhibition of indomethacin induced gastric lesion. The methanol extract showed low acute toxicity with minimum lethal dose of more than 3000 mg/kg, p.o. in mice. In conclusion, Zingiberis rhizoma exhibited antigastric and antiulcerative activity which might be attributable to inhibition of gastric secretion. It is revealed that the active component may be present in the hexane fraction.

• The Korean Journal of Physiology
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• v.22 no.2
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• pp.179-187
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• 1988

This study was conducted to investigate the effects of epinephrine and norepinephrine on basal gastric acid secretion and plasma gastrin and secretin concentration in the conscious rat. One hundred and eighty-four albino rats with gastric cannula were used after 18 hours or more of fast, with water ad libitum. In a restraint cage for collection of gastric juice, physiological saline (0.9% NaCl) was continuously infused into the jugular vein through a catheter for one hour at a rate of 1 ml/hr (control period). Immediately after the control period, epinephrine (1, 2, 4, 8 and $16{\mu}g/ml/hr)$, norepinephrine (1, 2, 4, 8 and $16{\mu}g/ml/hr)$ or physiological saline (1 ml/hr) was infused for another one hour. Gastric juice was collected at one hour interval for two hours infusion period. Adrenergic antagonists, phentolamine and propranolol were injected into the jugular vein 5 min prior to the infusion of epinephrine or norepinephrine at a dose of 0.2 mg/0.1 ml. Blood was sampled from the jugular vein for the radioimmunoassay of plasma gastrin and secretin after the collection of gastric juice. The results were as follows: 1) Both epinephrine and norephinephrine significantly increased gastric acid output in a dosedependent manner. 2) The effects of epinephrine and norepinephrine on the gastric acid secretion were antagonized by the pretreatment with phentolamine and propranolol. 3) Plasma gastrin and secretin concentrations were not significantly affected by the intravenous infusion of epinephrine and norepinephrine. It can be inferred from the above results that epinephrine and norepinephrine facilitate gastric acid secretion in conscious rats and the mechanism of which is attributed to ${\alpha}\;and\;{\beta}$ adrenergic receptors rather than gastrin and secretin.

• Journal of Dairy Science and Biotechnology
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• v.29 no.2
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• pp.17-23
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• 2011

The focus of this study was to clarify the relation between the nitric oxide (NO) production and cytokine expression including tumor necrosis factor-${\alpha}$ (TNF) and interleukin-6 (IL-6), and also investigated the effect of G-NANA (N-acylneuraminic acid isolates from glycomacropeptide) or S-NANA (Synthetic N-acylneuraminic acid) on LPS stimuli from RAW264.7 cell. The NANA is the predominant sialic acid found in mammalian cells and G-NANA is isolation of GMP (GMP is a valuable bioactive peptide with a varying degree of glycosylation including sialic acid). The lipopolysaccharide (LPS) of Gram-negative bacteria induces the expression of cytokines and potent inducers of inflammatory cytokines such as TNF-${\alpha}$ and IL-6. In this experiment, upon stimulation with increasing concentrations of chitosan, the LPS-stimulated TNF-${\alpha}$ and IL-6 secretion was significantly recovered with in the incubation media of RAW264.7 cells. Consistently, RT-PCR with mRNA and immunoblot analysis with anti-cytokine antiserum including TNF-${\alpha}$ and IL-6 showed that the amount of TNF-${\alpha}$ and IL-6 secretion in the incubation media recovered with the concentration of chitosan. The LPS-stimulated NO secretion was significantly recovered with in the 6 and 12 h incubation media of RAW264.7 cells, too. The recovery effect of G-NANA on IL-6 and NO secretion may be induced via the stimulus of TNF-${\alpha}$ in RAW264.7 cell. These results once again suggest that G-NANA may have the anti-inflammatory effect via the stimulus of TNF-${\alpha}$ in the LPS-stimulated inflammation in RAW264.7 cells.

• The Korean Journal of Pharmacology
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• v.29 no.2
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• pp.237-244
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• 1993

The effect of nicotine on the secretion of $[Met^{5}]-enkephalin$ (ME) in addition to proenkephalin A (proENK) mRNA levels and effects of indomethacin, nordihydroguaiaretic acid (NDGA), and captopril on nicotine-induced responses were studied in bovine adrenal medullary chromaffrin (BAMC) cells. Long-term exposure of BAMC cells to nicotine at a concentration of $10{\mu}M$ significantly increased proENK mRNA level and the secretion of ME into the medium. Treatment of BAMC cells with NDGA (a lipoxygenase inhibitor, $10{\mu}M$), indomethacin (a cycloooxygenase inhibitor) or captopril (an angiotensin converting enzyme inhibitor) alone did not affect ME secretion and proENK mRNA levels. The pretreatment of BAMC cells with NDGA inhibited the increased ME secretion and proENK mRNA level induced by nicotine. However, indomethacin and captopril did not affect nicotine-induced responses. Our results indicate that neuronal regulations of ME secretion and proENK mRNA level induced by nicotine in BAMC cells are in part mediated by a lipoxygenase-but not cyclooxygenase-and endogenous renin-angiotensin pathway.