• The Korean Journal of Pharmacology
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• v.12 no.1
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• pp.57-62
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• 1976

Using modified technique of Schmidt et al, as described previously (Korean J. Pharmacol 9 : 17, 1973), the stomach of female rats were perfused with physiological saline under urethane anesthesia. The acid-secretory response of the perfused stomach to i.v. hypertonic glucose (50%), casein hydrolysate (20%) or saline (6%) solution were studied with or without histamine or methacholine stimulation. A significant decrease of acid secretion from the rat stomach was induced by i.v. hypertonic glucose or saline solution. The histamine-stimulated acid secretion was also decreased by simultaneous administration of the hypertonic glucose or saline. However, methacholine-stimulated acid response was not affected by the hypertonic glucose. Intravenous infusion of 20% casein hydrolysate solution resulted in an increase in acid output from the stomach under histamine stimuli. These results lead to the conclusion that the inhibitory responses of acid secretion due to i.v. hypertonic glucose solution are brought through the effect of histaminergic, not cholnergic mechanism(s) in the gastric secretion.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.6
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• pp.503-510
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• 2001

Long-term treatment of cultured bovine adrenal medullary chromaffin (BAMC) cells with arachidonic acid $(100\;{\mu}M),$ angiotesnin II (100 nM), prostaglandin $E_2\;(PGE_2;\;10\;{\mu}M),$ veratridine $(2\;{\mu}M)$ or KCl (55 mM) for 24 hrs increased both norepinephrine and epinephrine levels in the supernatant. Pretreatment with staurosporine (10 nM), a protein kinase C (PKC) inhibitor, completely blocked increases of norepinephrine and epinephrine secretion induced by arachidonic acid, angiotensin II, $PGE_2,$ veratridine or KCl. In addition, K252a, another PKC inhibitor whose structure is similar to that of staurosporine, effectively attenuated both norepinephrine and epinephrine secretion induced by arachidonic acid. However, K252a did not affect the catecholamine secretion induced by angiotensin II, $PGE_2,$ veratridine or KCl. Our results suggest that staurosporine may inhibit long-term catecholamine secretion induced by various secretagogues in a mechanism other than inhibiting PKC signaling. Furthermore, long-term secretion of catecholamines induced by arachidonic acid may be dependent on PKC pathway.

• The Korean Journal of Physiology
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• v.14 no.2
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• pp.17-20
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• 1980

This study was undertaken to investigate the effect of the acidosis on the gastric acid secretion in the isolated whole stomach of the rat and the effect of prostaglandin $E_1$ on the gastric acid secretion influenced by the acidosis. Twenty-two male albino rats(Sprague-Dawley strain) were used. The isolated whole stomach from each rat was introduced into the Kreb's solution which was continuously gassed with $95%O_2-5%CO_2$ for 1 hour, after irrigation of the lumen with cold physiological saline$(4^{\circ}C)$. Thereafter, each stomach was irrigated again with 5% dextrose solution (pH 7.4, $37^{\circ}C$), and filled with the dextrose solution. All the stomachs with the dextrose solution were divided into 4 groups according to the Kreb's solutions in which each stomach was incubated for 30 min: 1) control group, in the pH 7.4 solution, 2) $PGE_1$ group, in the pH 7.4 solution containing $5\;{\mu}g/ml$ of $PGE_1$, 3) acid group, in the pH 7.0 solution, and 4) $acid+PGE_1$ group, in the pH 7.0 solution containing $5\;{\mu}g/ml$ of $PGE_1$. After incubatory period, the contents of each stomach were collected and centrifuged(1,500 rpm, room temperature) for 15 min. The acid output in the supernatant was determined with 0.012 N NaOH by means of autotitrator(Dosimat, Metrohm Herisau Co.) at pH 7.4. Results obtained were as follows: 1) The acid output of the acid group increased significantly in comparison with the control value. 2) The acid output of the $acid+PGE_1$ group decreased significantly in comparison with the acid group. It is inferred from the above results that the acidosis facilitates the gastric acid secretion and $PGE_1$ inhibits the gastric acid secretion induced by the acidosis.

• Biomedical Science Letters
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• v.26 no.4
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• pp.256-266
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• 2020

Carboxypeptidase D (CPD) is a zinc-dependent protease, which is highly expressed in macrophages, and is thought to participate in inflammatory processes. In the present study, we investigated the possible regulatory effect of all-trans retinoic acid (ATRA), which is an active form of vitamin A and plays a critical regulatory role in both the innate and adaptive immunity, on CPD expression and secretion in human monocytic THP-1 cells. CPD mRNA expression first increased, from a concentration as low as 10 nM ATRA to a maximum level of expression, at 1 μM. ATRA enhanced intracellular CPD expression in a time- and concentration-dependent manner but did not affect cell surface CPD expression. Interestingly, 9-cis-RA did not affect CPD expression. Additionally, an experiment with RAR/RXR selective agonist or antagonists demonstrated that ATRA-induced enhancement of CPD expression was RAR/RXR dependent. ATRA also enhanced CPD secretion from THP-1 cells; however, this enhancement was RAR/RXR-independent. The anti-inflammatory agent dexamethasone reversed ATRA-induced enhancement of CPD expression and secretion. Our results suggest ATRA exerts regulatory effects on expression and secretion of CPD in human monocytes, and ATRA-induced CPD secretion may be associated with inflammatory response.

• YAKHAK HOEJI
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• v.37 no.6
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• pp.581-590
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• 1993

In a preliminary screening of the plant extracts for the antigastritic action in rats, the extract of Aralia elata(Araliaceae) showed positive activity in HCI plus ethanol induced gastric lesion. Systematic fractions with hexane, chloroform, ethyl acetate and butanol resulted in the most patent activity with the butanol fraction: This butanol fraction at the oral dose of 200 mg/kg exhibited significant inhibition of absolute alcohol induced gastric lesion which was more potent than 100 mg/kg of cimetidine and had significant stimulation of mucus secretion. The butanol fraction showed significant decreases in the ulcer indices of Shay ulcers and inhibition of gastric juice secretion with acid output in pylorus-ligated stomachs of rats. It also suppressed the acetic acid induced gastric ulcer. These results might suggest that the butanol fraction had inhibitory action in gastric lesion and ulceration through inhibition of gastric acid secretion and stimulation of mucin secretion in the stomachs of rats.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.2
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• pp.197-204
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• 2017

In the present study, we tried to examine whether oleanolic acid regulates the activity, secretion and gene expression of matrix metalloproteinase-3 (MMP-3) in primary cultured rabbit articular chondrocytes, as well as the production of MMP-3 in the knee joint of rat to evaluate the potential chondroprotective effect of oleanolic acid. Rabbit articular chondrocytes were cultured in a monolayer, and reverse transcription-polymerase chain reaction (RT-PCR) was used to measure interleukin-$1{\beta}$ (IL-$1{\beta}$)-induced gene expression of MMP-3, MMP-1, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4), ADAMTS-5 and type II collagen. In rabbit articular chondrocytes, the effects of oleanolic acid on IL-$1{\beta}$-induced secretion and proteolytic activity of MMP-3 were investigated using western blot analysis and casein zymography, respectively. The effect of oleanolic acid on in vivo MMP-3 protein production was also examined, after intra-articular injection to the knee joint of rat. The results were as follows: (1) oleanolic acid inhibited the gene expression of MMP-3, MMP-1, MMP-13, ADAMTS-4, and ADAMTS-5, but increased the gene expression of type II collagen; (2) oleanolic acid reduced the secretion and proteolytic activity of MMP-3; (3) oleanolic acid suppressed the production of MMP-3 protein in vivo. These results suggest that oleanolic acid can regulate the activity, secretion and gene expression of MMP-3, by directly acting on articular chondrocytes.

• Laboraroty Animal Research
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• v.34 no.4
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• pp.140-146
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• 2018

Though bile acids have been well known as digestive juice, recent studies have demonstrated that bile acids bind to their endogenous receptors, including Farnesoid X receptor (FXR) and G protein-coupled bile acid receptor 1 (GPBAR1; TGR5) and serve as hormone to control various biological processes, including cholesterol/bile acid metabolism, glucose/lipid metabolism, immune responses, and energy metabolism. Deficiency of those bile acid receptors has been reported to induce diverse metabolic syndromes such as obesity, hyperlipidemia, hyperglycemia, and insulin resistance. As consistent, numerous studies have reported alteration of bile acid signaling pathways in type II diabetes patients. Interestingly, bile acids have shown to activate TGR5 in intestinal L cells and enhance secretion of glucagon-like peptide 1 (GLP-1) to potentiate insulin secretion in response to glucose. Moreover, FXR has been shown to crosstalk with TGR5 to control GLP-1 secretion. Altogether, bile acid receptors, FXR and TGR5 are potent therapeutic targets for the treatment of metabolic diseases, including type II diabetes.

• The Journal of Korean Medicine
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• v.42 no.4
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• pp.150-163
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• 2021

Objectives: The purpose of this study was to confirm the effects of Liriope platyphylla extract on relieving Gastroesophageal reflux disease (GERD) through regulation of acid secretion. Methods: 8-week-old ICR mice were divided into untreated control group (Ctrl), GERD elecitation group (GERDE), Omeprazole administrate group before GERD elicitation (OMA), and Liriope platyphylla extract administrate group before GERD elicitation (LPA). After inducing GERD, gross observation and histological examination were performed and ATP6V1B1 (ATPase H+ Transporting V1 Subunit B1), GRPR (Gastrin-releasing peptide receptor), COX-1 (Cyclooxygenase 1), 8-OHdG (8-hydroxy-2'-deoxyguanosine), Cathelicidin, p-JNK (phospho c-Jun N-terminal kinase) were observed to confirm the damage defense effect of the esophageal mucosa, acid secretion regulation, antioxidant, anti-inflammatory, mucosal protection, and apoptosis regulation Results: OMA and LPA showed lower levels of damage compared to GERDE in gross observation and histological examination. ATP6V1B1, GRPR, and 8-OHdG showed lower positive reactions in OMA and LPA than in GERDE. COX-1 were less positive in GERDE and OMA than in Ctrl, but showed higher secretion in LPA than in Ctrl. Cathelicidin showed a decreased positive reaction in GERDE, OMA and LPA compared to Ctrl, but the decrease in positive reaction was smaller in OMA and LPA compared to GERDE. p-JNK showed increased positive reaction in GERDE, OMA and LPA than in Ctrl, but the increase in the positive reaction was smaller in the OMA and LPA compared to GERDE. Conclusions: The effects of Liriope platyphylla extract on esophageal mucosal damage protection, acid secretion regulation, antioxidant, anti-inflammatory, mucosal protection and apoptosis regulation were confirmed.

• Archives of Pharmacal Research
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• v.25 no.1
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• pp.61-66
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• 2002

From our previous result that Panax ginseng head extract had inhibition of gastric damages, the extract was fractionated. Among the hexane, chloroform, butanol and water fractions, butanol fraction Showed the most potent inhibition of HCl.ethanol-induced gastric lesion, aspirin-induced gastric ulcer, acetic acid-induced ulcer and Shay ulcer. Butanol fraction showed significant increase in mucin secretion, and inhibited malondialdehyde (MDA) and $H^{+}/K^{+}ATPase$ activity in the stomach. This results indicate that the effectiveness of the fraction on gastric damages might be related to inhibition of acid secretion, increment of mucin secretion and antioxidant property.

• Animal cells and systems
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• v.1 no.1
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• pp.81-86
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• 1997

We studied the mechanism of arachidonic acid on the secretion of a neurotransmitter in rat pheochromocytoma PC12 cells. Arachidonic acid inhibited the 70 mM $K^+$-induced secretion of norepinephrine. Arachidonic acid also inhibited the 70 mM $K^+$-induced $Ca^{2+}$ mobilization which is due to the opening of the voltage-sensitive $Ca^{2+}$ channels (VSCC). Both the half maximal inhibitory concentration ($IC_{50}$) of the norepinephrine secretion and VSCC coincided at 30 uM. The major oxidized metabolites of arachidonic acid, prostaglandins did not mimic the inhibitory effect of arachidonic acid. Nordihydroguaiaretic acid (NDGA) and indomethacin which are inhibitors of lipoxygenase and cyclooxygenase, respectively, did not block the inhibitory effect of arachidonic acid. The results suggest that arachidonic acid serves as a signal itself, not in the form of metabolites. The pretreatment of various $K^+$ channel blockers such as 4-aminopyridine, tetraethylarnmonium, glipizide, or glibenclamide also did not show any effect on the inhibitory effect of arachidonic acid. Through these results we suggest that arachidonic acid regulates VSCC directly and affects the secretion of neurotransmitters.