Escitalopram is one of selective serotonin reuptake inhibitor antidepressants. As an S-enantiomer of citalopram, it shows better therapeutic outcome in depression and anxiety disorder treatment because it has higher selectivity for serotonin reuptake transporter than citalopram. The objective of this study was to determine the direct inhibitory effect of escitalopram on 5-hydroxytryptamine type 3 ($5-HT_3$) receptor currents and study its blocking mechanism to explore additional pharmacological effects of escitalopram through $5-HT_3$ receptors. Using a wholecell voltage clamp method, we recorded currents of $5-HT_3$ receptors when 5-HT was applied alone or co-applied with escitalopram in cultured NCB-20 neuroblastoma cells known to express $5-HT_3$ receptors. 5-HT induced currents were inhibited by escitalopram in a concentration-dependent manner. $EC_{50}$ of 5-HT on $5-HT_3$ receptor currents was increased by escitalopram while the maximal peak amplitude was reduced by escitalopram. The inhibitory effect of escitalopram was voltage independent. Escitalopram worked more effectively when it was co-applied with 5-HT than pre-application of escitalopram. Moreover, escitalopram showed fast association and dissociation to the open state of $5-HT_3$ receptor channel with accelerating receptor desensitization. Although escitalopram accelerated $5-HT_3$ receptor desensitization, it did not change the time course of desensitization recovery. These results suggest that escitalopram can inhibit $5-HT_3$ receptor currents in a non-competitive manner with the mechanism of open channel blocking.
Tak, Mi-Jin;Tark, Myoung-Rim;Kang, Kyoung-Hwa;Ko, Woo-Shin;Yoon, Hwa-Jung
The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
/
v.23
no.1
/
pp.118-134
/
2010
Objective: Yang Geouk San Hwa - Tang (YGSHT) has been widely used in Sasang Constitutional Medicine of Korea for treatment of acute inflammatory symptom, such as palatine tonsillitis, polydipsia, headache, papule, pimple however, the mechanism of its anti-inflammatory activity has not been clarified. In this study, therefore, we investigated the mechanism of the inhibitory effect of YGSHT on LPS-induced inflammation. Materials and methods: The effect of YGSHT was analyzed by ELISA, RT-PCR and Western blotting in LPS-stimulated RAW264.7 cells. Results: We found that YGSHT suppressed not only the production of pre-inflammatory cytokines (IL-$1{\beta}$ and TNF-$\alpha$), the generation of nitric oxide (NO) and prostaglandin E (PGE)2, but also the mRNA expression of pre-inflammatory cytokines, inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX)-2. Furthermore, YGSHT was shown to inhibit the phosphorylation of ERK1/2 and JNK1/2 and the activation and translocation of NF-kB from cytosol to nuclear in LPS-stimulated RAW264.7 cells. Conclusions: These results suggest that YGSHT exerts an anti-inflammatory effect through the regulation of the ERK1/2 and JNK1/2 pathway and NF-kB pathway, thereby decreasing production of pre-inflammatory cytokines, NO, and PGE2.
The purpose of this study was to determine whether bromocriptine affects the catecholamines (CA) secretion evoked in isolated perfused rat adrenal glands, by cholinergic stimulation, membrane depolarization and calcium mobilization, and to establish the mechanism of its action. The perfusion of bromocriptine ($1~10{\;}{\mu}M$) into an adrenal vein, for 60 min, produced relatively dose-dependent inhibition in the secretion of catecholamines (CA) evoked by acetylcholine (ACh, 5.32 mM), DMPP ($100{\;}{\mu}M$ for 2 min), McN-A-343 ($100{\;}{\mu}M$ for 2 min), cyclopiazonic acid (CPA, $10{\;}{\mu}M$ for 4 min) and Bay-K-8644 ($10{\;}{\mu}M$ for 4 min). High $K^+$ (56 mM)-evoked CA release was also inhibited, although not in a dose-dependent fashion. Also, in the presence of apomorphine ($100{\;}{\mu}M$), which is also known to be a selective $D_2$-agonist, the CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly depressed. However, in adrenal glands preloaded with bromocriptine ($3{\;}{\mu}M$) in the presence of metoclopramide ($15{\;}{\mu}M$), a selective $D_2$-antagonist, the CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid considerably recovered as compared to that of bromocriptine only. Taken together, these results suggest that bromocriptine can inhibit the CA secretion evoked by stimulation of cholinergic receptors, as well as by membrane depolarization, in the perfused rat adrenal medulla. It is thought this inhibitory effect of bromocriptine may be mediated by inhibiting the influx of extracellular calcium and the release from intracellular calcium stores, through the activation of dopaminergic $D_2$-receptors located in the rat adrenomedullary chromaffin cells. Furthermore, these findings also suggest that the dopaminergic $D_2$-receptors may play an important role in regulating adrenomedullary CA secretion.
Ethanol often causes critical health problems by altering the neuronal activities of the central and peripheral nerve systems. One of the cellular targets of ethanol is the plasma membrane proteins including ion channels and receptors. Recently, we reported that ethanol elevates membrane excitability in sympathetic neurons by inhibiting Kv7.2/7.3 channels in a cell type-specific manner. Even though our studies revealed that the inhibitory effects of ethanol on the Kv7.2/7.3 channel was diminished by the increase of plasma membrane phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), the molecular mechanism of ethanol on Kv7.2/7.3 channel inhibition remains unclear. By investigating the kinetics of Kv7.2/7.3 current in high K+ solution, we found that ethanol inhibited Kv7.2/7.3 channels through a mechanism distinct from that of tetraethylammonium (TEA) which enters into the pore and blocks the gate of the channels. Using a non-stationary noise analysis (NSNA), we demonstrated that the inhibitory effect of ethanol is the result of reduction of open probability (PO) of the Kv7.2/7.3 channel, but not of a single channel current (i) or channel number (N). Finally, ethanol selectively facilitated the kinetics of Kv7.2 current suppression by voltage-sensing phosphatase (VSP)-induced PI(4,5)P2 depletion, while it slowed down Kv7.2 current recovery from the VSP-induced inhibition. Together our results suggest that ethanol regulates neuronal activity through the reduction of open probability and PI(4,5)P2 sensitivity of Kv7.2/7.3 channels.
Shin, Jung-Hae;Kwon, Hyuk-Woo;Irfan, Muhammad;Rhee, Man Hee;Lee, Dong-Ha
Journal of Ginseng Research
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v.45
no.4
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pp.490-497
/
2021
Background and objective: Synthetic ginsenoside compounds G-Rp (1,3, and 4) and natural ginsenosides in Panax ginseng 20(S)-Rg3, Rg6, F4 and Ro have inhibitory actions on human platelets. However, the inhibitory mechanism of ginsenoside Rk1 (G-Rk1) is still unclear thus, we initiated investigation of the anti-platelet mechanism by G-Rk1 from Panax ginseng. Methodology: Our study focused to investigate the action of G-Rk1 on agonist-stimulated human platelet aggregation, inhibition of platelet signaling molecules such as fibrinogen binding with integrin αIIbβ3 using flow cytometry, intracellular calcium mobilization, fibronectin adhesion, dense granule secretion, and thromboxane B2 secretion. Thrombin-induced clot retraction was also observed in human platelets. Key Results: Collagen, thrombin, and U46619-stimulated human platelet aggregation were dose-dependently inhibited by G-Rk1, while it demonstrated a more effective suppression on collagen-stimulated platelet aggregation using human platelets. Moreover, G-Rk1 suppressed collagen-induced elevation of Ca2+ release from endoplasmic reticulum, granule release, and αIIbβ3 activity without any cytotoxicity. Conclusions and implications: These results indicate that G-Rk1 possess strong anti-platelet effect, proposing a new drug candidate for treatment and prevention of platelet-mediated thrombosis in cardiovascular disease.
Objective : Infectious diseases are a growing problem worldwide by Methicillin-resistant Staphylococcus aureus (MRSA). Daehwangmokdan-tang is one of the oriental medicine prescriptions contained in Principles and Practice of Eastern Medicine. This study investigated the antibacterial activity of EtOH 70% extracts of Daehwangmokdan-tang (DMT) which prescription is composed of oriental medicine against MRSA. Methods : The antimicrobial activity and active concentration of MRSA were verified by measuring the minimum inhibitory concentration (MIC) of DMT. In addition, the effects of the disease were checked by treating the existing antibiotics and large ethanol extract in parallel, and the extent of growth suppression was checked over time. In addition, cell membrane permeability experiment confirmed the effect of large DMT on the immunity mechanism of MRSA. Results : TThe minimum inhibitory concentration of DMT against MRSA is 500 ~ 2000 ㎍/㎖ by broth dilution method. In the checkerboard method, the combinations of DMT with antibiotics has partial synergistic effect or synergy effect and DMT markedly reduced the MICs of the antibiotics oxacillin (OX), gentamicin (GEN) against MRSA. In the inhibition of resistance mechanism of DMT against MRSA, the expression of resistance gene and protein about β-lactam antibiotic was reduced. Also, we observed the effect of DMT about cell membrane permeability against MRSA, and confirmed that DMT suppressed growth of strains by increasing cell membrane permeability and energy metabolism. Conclusion : Basis on the result, we speculate that DMT may be useful for the treatment of MRSA infections when used in combination with β-lactam antibiotic.
Hyun-Jin Jang;Soon Lee;Eunmi Hong;Kyung June Yim;Yong-Soo Choi;Ji Young Jung;Z-Hun Kim
Journal of Microbiology and Biotechnology
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v.33
no.4
/
pp.449-462
/
2023
Previously, we confirmed that Mychonastes sp. 246 methanolic extract (ME) markedly reduced the viability of BxPC-3 human pancreatic cancer cells. However, the underlying mechanism ME remained unclear. Hence, we attempted to elucidate the anticancer effect of ME on BxPC-3 human pancreatic cancer cells. First, we investigated the components of ME and their cytotoxicity in normal cells. Then, we confirmed the G1 phase arrest mediated growth inhibitory effect of ME using a cell counting assay and cell cycle analysis. Moreover, we found that the migration-inhibitory effect of ME using a Transwell migration assay. Through RNA sequencing, Gene Ontology-based network analysis, and western blotting, we explored the intracellular mechanisms of ME in BxPC-3 cells. ME modulated the intracellular energy metabolism-related pathway by altering the mRNA levels of IGFBP3 and PPARGC1A in BxPC-3 cells and reduced PI3K and mTOR phosphorylation by upregulating IGFBP3 and 4E-BP1 expression. Finally, we verified that ME reduced the growth of three-dimensional (3D) pancreatic cancer spheroids. Our study demonstrates that ME suppresses pancreatic cancer proliferation through the IGFBP3-PI3K-mTOR signaling pathway. This is the first study on the anticancer effect of the ME against pancreatic cancer, suggesting therapeutic possibilities and the underlying mechanism of ME action.
Many in-depth reviews related to regulations of prolactin secretion are available. We will, therefore, focus on controversial aspects using personal opinion in this review. The neuroendocrine control of prolactin secretion from the anterior pituitary gland involves multiple factors including prolactin-release inhibiting factor (PIF) and prolactin releasing factor (PRF). The PIF exerts a tonic inhibitory control in the physiological conditions. The PIF should be able to effectively inhibit prolactin release or a lifetime, but the inhibitory action of dopamine cannot be sustained for a long period of time. Perifusion of a high concentration of dopamine (l ,000 nM) could not sustain inhibitory action on prolactin release but when a small amount of ascorbic acid (0.1 mM) is added in a low concentration of dopamine (3 nM) solution, prolactin release was inhibited for a long period. Ascorbate is essential for dopamine action to inhibit prolactin release. We have, therefore, concluded that the PIF is dopamine plus ascorbate. The major transduction system for dopamine to inhibit prolactin release is the adenylyl cyclase system. Dopamine decreases cyclic AMP concentration by inhibiting adenylyl cyclase, and cyclic AMP stimulates prolactin release. However, the inhibitory mechanism of dopamine on prolactin release is much more complex than simple inhibition of CAMP production. The dopamine not only inhibits cyclic AMP synthesis but also inhibits prolactin release by acting on a link(s) after the CAMP event in a chain reaction for inhibiting prolactin release. Low concentrations of dopamine stimulate prolactin release. Lactotropes are made of several different subtypes of cells and several different dopamine receptors are found in pituitary. The inhibitory and stimulatory actions induced by dopamine can be generated by different subtype of receptors. The GH$_4$ZR$_7$ cells express only the short isoform (D$_{2s}$) of the dopamine receptor, as a result of transfecting the D$_{2s}$ receptors into GH$_4$C$_1$ cells which do not express any dopamine receptors. When dopamine stimulates or inhibits prolactin release in GH$_4$ZR$_7$ cells, it is clear that the dopamine should act on dopamine D$_{2s}$ receptors since there is no other dopamine receptor in the GH$_4$ZR$_7$. Dopamine is able to stimulate prolactin release in a relatively low concentration while it inhibits in a high concentration in GH$_4$ZR$_7$. These observations indicate that the dopamine D$_2$ receptor can activate stimulatory and/or inhibitory transduction system depending upon dopamine concentrations.
In order to investigate the protective effect of Samduhaejungtang-gamibang on the liver injury of rats induced by $CCl_4$ and d-galactosamine, the serum transaminase(GOT& GPT) alkaline phosphatase(ALP), lactic dehydrogenase(LDH) for enzyme activities and triglyceride, total bilirubin amounts for serum component were measured. All animals were divided into 4 groups, those were normal group(untreated), control group(treated with vehicle 0.9% Saline solution), sample Ⅰ group(1500mg/kg administrated), sample Ⅱ group(3000mg/kg administrated). The results were as follows: 1. The inhibitory effects of the serum GOT activities in rats induced by $CCl_4$ were noted in sample Ⅱ group(p<0.01). In serum GPT activities, sample Ⅱ group(p<0.05) only showed the inhibitory effects. 2. The inhibitory effects of the serum ALP activities in rats induced by $CCl_4$ were noted in sample Ⅱ group(p<0.01) 3. The inhibitory effects of the serum LPH activities in rats induced by $CCl_4$ were noted in sample Ⅱ group, but it is not recognized statistically. 4. The increases effects of the serum triglyceride content level in rats induced by $CCl_4$ were inhibited in both sample Ⅰ group(p<0.05) and sample Ⅱ group(p<0.01) 5. The increases effects of the serum total bilirubin content level in rats induced by $CCl_4$ were inhibited in sample Ⅱ group(p<0.05) 6. The inhibitory effects of the serum GOT, GPT activities in rats induced by d-galactosamine were noted in sample Ⅱ group (p<0.001), but sample Ⅰ group was not recognized. 7. The signiticantly inhibitory effects of in the serum LDH activities in rats induced by d-galactosamine were noted in both sample Ⅰ group(p<0.05) and sample Ⅱ group (p<0.001) 8. The increases of the serum ALP content level in rats induced by d-galactosamine were inhibited in sample Ⅱ group(p<0.05) 9. The increases of the serum total bilirubin content level in rats induced d-galactosamine were inhibited in sample Ⅱgroup(p<0.05) According to the above results, it is considered that Samduhaejungtang-gamibang has protective effect against liver injury in rats induced by $CCl_4$ and d-galactosamine. So it is required to study about the actions of mutual relation of medicines and patho-mechanism by experiment.
Hyaluronidase inhibitory activity as inflammatory factor of Koreinsis chinensis leaf ethanol extract was showed higher inhibitory activity than water extract. 29.5% inhibitory activity was shown at concentration of $200{\mu}g/mL$ phenolics. Lipopolysaccharide (LPS)-stimulated Raw 264.7 cells were treated with different concentrations ($5-25{\mu}g/mL$) of Koreinsis chinensis leaf extract and the amount of nitric oxide (NO) was determined; LPS-treated cells produced 3 times more NO than non-LPS treated cells. Moreover, the NO production in cells treated with Koreinsis chinensis leaf extract showed inhibitory effect in a concentration-dependent manner. Due to the stimulant-induced NO production is regulated by the inducible nitric oxide synthase (iNOS), we determined the iNOS protein level to elucidate the mechanism by which the NO production was inhibited. It was reduced by 40% with a Koreinsis chinensis leaf extract concentration of $25{\mu}g/mL$ and identified iNOS inhibition in dose-dependent manner. The prostaglandin $E_2$ production in cells treated with Koreinsis chinensis leaf extract was reduced by 26.2% at concentration of $25{\mu}g/mL$. The protein expression of cyclooxygenase-2 in LPS-treated Raw 264.7 cells was inhibited by 64% at $25{\mu}g/mL$ of Koreinsis chinensis leaf extract. Koreinsis chinensis leaf extract had a concentration-dependent inhibitory effect on the production of tumor necrosis factor-${\alpha}$ and interleukin-6 as pro-inflammatory cytokine in LPS-treated Raw 264.7 cells at $25{\mu}g/mL$ of Koreinsis chinensis leaf extract. Their levels were decreased by 61.7 and 62% respectively.
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