• Journal of Ginseng Research
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• v.46 no.2
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• pp.225-234
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• 2022

Background: Ginseng, officially known as Panax ginseng Meyer, has been traditionally used as a medicinal herb, particularly in Asia. Ginseng is propagated from seeds; however, seed germination is challenging, especially in its natural environment on farms. The seeds typically exhibit morphophysiological dormancy and require release from both morphological and physiological dormancy before germination. Although some studies have proposed methods for increasing seed germination rates, the underlying mechanisms of its dormancy release process remain unclear. Here, we investigated metabolic alterations during dehiscence in P. ginseng to determine their potential roles in dormancy release. Methods: We compared the ginseng seed metabolome before and after dehiscence and the ginsenoside and phytosterol compositions of the seeds in both periods in the presence of related enzymes. Results: After seed dehiscence, the sugar, amino acid, and squalene concentrations were significantly altered, phytosterols associated with the stigmasterol biosynthesis pathway were increased, while ginsenoside and brassinosteroid levels were not significantly altered. In addition, squalene epoxidase, cycloartenol synthase, 24-methylenesterol C-methyltransferase, and the stigmasterol biosynthesis pathway were activated. Conclusion: Overall, our findings suggest that morphological activities that facilitate ginseng seed growth are the primary phenomena occurring during the dehiscence process. This study improves the understanding of P. ginseng germination processes and promotes further research of its germination and cultivation.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.279.1-279.1
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• 2002

Accumulation of ceramide mass in MCF-7 cells by the anti-cancer agent. paclitaxel. was found to occur primarily due to activation of the de novo synthesis pathway. Morever. the addition of paclitaxel resulted in the accumulation of ceramide, which was followed by a prolonged arachidonic acid release. Participation of ceramide de novo pathway in arachidonate signaling was detected since L-cycloserine, an inhibitor of de novo synthesis, was able to inhibit the paclitaxel-induced AA release and cytotoxicity. (omitted)

• Archives of Pharmacal Research
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• v.28 no.1
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• pp.73-80
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• 2005

The effect of capsaicin on apoptotic cell death was investigated in HepG2 human hepatoma cells. Capsaicin induced apoptosis in time- and dose-dependent manners. Capsaicin induced a rapid and sustained increase in intracellular $Ca^{2+}$ concentration, and BAPTA, an intracellular $Ca^{2+}$ chelator, significantly inhibited capsaicin-induced apoptosis. The capsaicin-induced increase in the intracellular $Ca^{2+}$ and apoptosis were not significantly affected by the extracellular $Ca^{2+}$ chelation with EGTA, whereas blockers of intracellular $Ca^{2+}$ release (dantrolene) and phospholipase C inhibitors, U-73122 and manoalide, profoundly reduced the capsaicin effects. Interestingly, treatment with the vanilloid receptor antagonist, capsazepine, did not inhibit either the increased capsaicin-induced $Ca^{2+}$ or apoptosis. Collectively, these results suggest that the capsaicin-induced apoptosis in the HepG2 cells may result from the activation of a PLC-dependent intracellular $Ca^{2+}$ release pathway, and it is further suggested that capsaicin may be valuable for the therapeutic intervention of human hepatomas.

• Archives of Pharmacal Research
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• v.21 no.2
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• pp.113-119
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• 1998

Changes in the release and uptake of glutamate in cerebellar granule and glial cells of offspring of lead-exposed mothers were determined. In cultured cerebellar granule cells exposed to lead for 5 days, glutamate release was less influenced upon N-methyl-D-aspartate (NMDA) stimulation than that in the control. Although the NMDA-stimulated release of glutamate in cerebellar granule cells prepared from lead-exposed first generation pups was not different from that of the control group, the S-nitroso-N-acetylpenicillamine (SNAP)-stimulated release of glutamate in cerebellar granule cells obtained from lead-treated pups was less elevated than that in the control. Furthermore, in cerebellar granule cells obtained from lead-exposed second generations pups, glutamate release did not respond to both NMDA and SNAP stimulation. In cerebellar glial cells exposed to lead, the basal glutamate uptake was not changed. However, the L-trans-pyrollidine-2,4-dicarboxylic acid (PDC)-blocking effects was significantly reduced. In glial cells obtained from lead-exposed pups, the glutamate uptake was also less blocked by PDC than that in the control. Further decreases in PDC-blocking effects were observed in cerebellar glial cells obtained from lead-treated second generation pups compared to those from the control group. These results indicate that lead exposure induces the changes in the sensitivities of the glutamate release and uptake transporter. In addition, these results suggest that lead exposure might affect the intracellular signalling pathway and transmission in glutamatergic nervous system.

• Journal of Applied Biological Chemistry
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• v.64 no.2
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• pp.105-112
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• 2021

Excessive accumulation of the amyloid beta (Aβ) peptide has been implicated in the pathogenesis of Alzheimer's disease (AD). Paeonia lactiflora (PL) has been used in treatments of several conditions such as inflammation, arthritis, and cognitive impairment. The purpose of this study was to investigate the neuroprotective effect and mechanisms of PL and its active compound, paeoniflorin (PF), on Aβ_25-35-induced neurotoxicity in SH-SY5Y cells. We evaluated cell viability, lactate dehydrogenase (LDH) release and reactive oxygen species (ROS) production. Furthermore, underlying mechanism of PL and PF on the regulation of amyloidogenic pathway was analyzed by Western blotting. In our results, Aβ_25-35-induced neuronal cell loss was observed, whereas treatment with PL (10, 50, and 100 ㎍/mL) and PF (1, 5, and 10 ㎍/mL) significantly elevated the cell viability, and decreased LDH release and ROS production. In addition, exposure of SH-SY5Y cells to Aβ_25-35 significantly increased the protein levels of amyloid precursor protein (APP)-C-terminal fragment β, β-site APP-cleaving enzyme, and presenilin-1 and -2. However, treatment with PL and PF inhibited the amyloidogenic pathway via the down-regulation of those protein expressions. Taken together, our results indicate that PL, and its active compound PF, could protect SH-SY5Y cells against Aβ_25-35-induced cell neurotoxicity by attenuating LDH release and ROS production, and these effects may be attributed to regulation of amyloidogenic pathway-related protein expression. In conclusion, PL and PF could be a potential to prevent neurodegenerative disorders such as AD.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.222.2-223
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• 2003

Renal dipeptidase (RDPase, EC 3.4.13.19), an ectoenzyme of renal proximal tubules, is covalently bound to outer leaflet of lipid bilayer via glycosylphosphatidylinositol (GPI)-anchor. Chitin is a major component of the shells of crustacea such as crab, shrimp and crawfish. This study was conducted to examine the effect of chitosan on RDPase release from renal proximal tubules. Nitric oxide (NO), highly reactive free radical, inhibits the release of RDPase from porcine proximal tubules. (omitted)

• Korean Journal of Veterinary Research
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• v.39 no.1
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• pp.55-61
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• 1999

The present experiments were performed to examine the effects of acetylcholine (ACh) and carbachol (CC) on thyroxine ($T_4$) release and any possible relation between inhibition of $T_4$ release and signaling pathway in guinea pig thyroids. The thyroids were incubated in the medium containing the test agents, samples of the medium were assayed for $T_4$ by EIA kits. ACh and CC inhibited the TSH-stimulated $T_4$ release. These inhibition were reversed by atropine, but not by d-tubocurarine. The inhibitory effects of ACh on $T_4$ release were prevented by $M_{1^-}$ and $M_{3^-}$muscarinic antagonists and its inhibition was also slightly reversed by $M_{2^-}$ and $M_{4^-}$muscarinic antagonists. R59022, like ACh and CC, also inhibited the TSH-stimulated $T_4$ release. This inhibition was reversed by protein kinase C inhibitor and $Ca^{2+}$ channel blocker. The present study suggests that cholinergic inhibition of $T_4$ release from thyroids can be induced mainly by activation of the $M_{1^-}$ or $M_{3^-}$ receptors and that it is mediated through the muscarinic receptorstimulated protein kinase C activation.

• Biomedical Science Letters
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• v.27 no.3
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• pp.170-176
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• 2021

Thapsigargin (TG), a sarco/endoplasmic reticulum (ER) Ca²⁺-ATPase (SERCA) inhibitor, has been widely used as an agonist for platelet aggregation for decades. In this study, we investigated the effect of TG on the release of lactate dehydrogenase (LDH) for platelets and elucidated its mechanism. Platelet LDH release and platelet aggregation were increased by TG treatment; 1,000 nM of TG induced the complete lysis of platelets. Other agonists such as collagen (2.5 ㎍/mL), thrombin (0.1 U/mL), and ADP (10 mM) did not induce significant platelet LDH release despite platelet aggregation. Finally, we investigated the effects of pharmacological inhibitors on TG-induced platelet aggregation and LDH release. SP600125, a JNK inhibitor, and LY294002, a PI-3K inhibitor, inhibited TG-induced platelet LDH release but not platelet aggregation. Forskolin, an adenylyl cyclase activator, also inhibited LDH release without affecting platelet aggregation by TG. These results suggest that the TG-induced platelet aggregation was accompanied by LDH release but regulated by a different signaling pathway.

• Journal of Radiation Protection and Research
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• v.10 no.1
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• pp.50-63
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• 1985

A derivation of new release limit, named Derived Release Limit(DRL), into the atomsphere from a reference nuclear power plant has been performed on the basis of the new system of dose limitation recommended by the ICRP, instead of the (MPC)a limit which has been currently used until now as a general standard for radioactive effluents in Korea. In DRL Calculation, a Concentration Factor Method was applied, in which the concentrations of long-term routinely released radionuclides were in equilibrium with dose in environment under the steady state condition. The analytical model used in the exposure pathway analysis was the one which has been suggested by the USNRC and the exposure limits applied in this analysis were those recommended by the USEPA lately. In the exposure pathway analysis, all of the pathways are not considered and some may be excluded either because they are not applicable or their contribution to the exposure is insignificant compared with other pathways. In case, the environmental model developed in this study was applied to the Kori nuclear power plant as the reference power plant, the highest DRL value was calculated to be as $9.10{\times}10^6Ci/yr$ for Kr-85 in external whole body exposure from the semi-infinite radioactive cloud, while the lowest DRL value was observed 3.64Ci/yr for Co-60 in external whole body exposure from the contaminated ground, by the radioactive particulates. The most critical exposure pathway to an individual in the unrestricted area of interest (Kilchun-Ri, 1.3 km to the north of the release point) seems to be the exposure pathway from the contaminated ground and the most critical radionuclide in all pathways appears to be Co-60 in the same pathway. When comparing the actual release rate from KNU-l in 1982 with the DRL's obtained here the release of radionuclides from KNU-1 were much lower than the DRL's and it could be conclued that the exposure to an individual had been kept below the exposure limits recommended by the USEPA.

• The Journal of Korean Medicine
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• v.27 no.4
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• pp.74-83
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• 2006

Ssanghwatang (SHT) has been known to prove effective in the treatment for erectile dysfunction (ED), and its modified formula is widely used in clinical practice. However, its fundamental mechanism of action is not clearly known. It is well known that endothelial cells can achieve the relaxation of vascular smooth muscles by the release of nitric oxide (NO). NO is synthesized by the enzyme NO synthase (NOS) from L-arginine and oxygen. It is widely accepted that NO plays an important role in the relaxation of corpus cavernous smooth muscle and vasculature. In addition, in terms of the penile erection, the NO/cGMP pathway is more potent than the PCE1/cAMP pathway. The main purpose of the present study was to investigate the mechanism of the erectile effects of SHT by focusing on its direct effects on corpus cavernous smooth muscle cells. We investigated the NOS activity, nitrite concentration and cGMP levels in rat corpus cavernous smooth muscle cell lines activated by SHT extracts. Furthermore, we evaluated the effect of SHT extracts on penile smooth muscle relaxation following oral administration of SHT extract powder to rats by the dosage of 1 g/kg over fifteen days. As a result, we found that SHT stimulated NO release. NOS activity and cGMP levels were increased by SHT respectively. Furthermore, SHT relaxed the corpus cavernous smooth muscle. These results are consistent with the concept that penile erection by SHT is carried out through the NO/cGMP pathway. In conclusion, the present study shows that SHT increases the NOS activity, synthesizes NO and augments the cGMP, which mediates penile erection. Further determination of the SHT mechanism related with the NO/cGMP pathway strongly indicates that SHT can be used as a remedy for erectile impotence.