• The Korean Journal of Physiology and Pharmacology
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• v.20 no.3
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• pp.237-243
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• 2016

Oleanolic acid (OA) has a wide variety of bioactivities such as hepatoprotective, anti-inflammatory and anti-cancer activity and is used for medicinal purposes in many Asian countries. In the present study, the effect of OA on induction of autophagy in human hepatocellular carcinoma HepG2 and SMC7721 cells and the related mechanisms were investigated. MTT assay showed that OA significantly inhibited HepG2 and SMC7721 cells growth. OA treatment enhanced formation of autophagic vacuoles as revealed by monodansylcadaverine (MDC) staining. At the same time, increasing punctuate distribution of microtubule-associated protein 1 light chain 3 (LC3) and an increasing ratio of LC3-II to LC3-I were also triggered by OA incubation. In addition, OA-induced cell death was significantly inhibited by autophagy inhibitors 3-methyladenine (3-MA) and chloroquine (CQ) pretreatment. And we found out that OA can suppress the PI3K/Akt1/mTOR signaling pathway. Furthermore, our data suggested that OA-triggered autophagy was ROS-dependent as demonstrated by elevated cellular ROS levels by OA treatment. When ROS was cleared by N-acetylcysteine (NAC), OA-induced LC3-II convertsion and cell death were all reversed. Taken together, our results suggest that OA exerts anticancer effect via autophagic cell death in hepatocellular carcinoma.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.9 no.1
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• pp.61-68
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• 1976

For the artificial precocious breeding of abalone effects of changes in environmental parameters, water temperature and light period, on the induction of spawning have been studied. Subtidal specimens of Haliotis discus hannai were collected irregularly for 6 times from April to June 1975 in Chungmu Bay near Jukdo Island, the southern coast of Korea. One hundred and fifty specimens were reared in 4 aquarium tanks in the laboratory and in a creel submerged in the sea during the period of 60 days from April 24 to June 23, 1975. The all groups kept in the four tanks and a creel showed very high spawning rates $(70\~100\%)$, compared to those inhabited the natural environment at sea until right before the spawning time $(0\~50\%,\;average\;16.4\%)$. From the results of the present induced spawning, the parameters can be discussed as follows: It seems likely that photoenvironment may stimulate to produce and secrete some internal substances which may concern to giving the fertilizing ability to the eggs before spawning and to inducing spawning, but the temperature may not be a factor for this concern. For effective precocious breeding, it seems to require that abalones are to be realoed under controlled conditions of darkness below 2,000 lux even during day time for more than 60 days before inducing spawning.

• Journal of Periodontal and Implant Science
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• v.50 no.5
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• pp.291-302
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• 2020

Purpose: The objective of this study was to investigate whether phelligridin D could reduce glucose-induced oxidative stress, attenuate the resulting inflammatory response, and restore the function of human periodontal ligament cells (HPDLCs). Methods: Primary HPDLCs were isolated from healthy human teeth and cultured. To investigate the effect of phelligridin D on glucose-induced oxidative stress, HPDLCs were treated with phelligridin D, various concentrations of glucose, and glucose oxidase. Glucose-induced oxidative stress, inflammatory molecules, osteoblast differentiation, and mineralization of the HPDLCs were measured by hydrogen peroxide (H₂O₂) generation, cellular viability, alkaline phosphatase (ALP) activity, alizarin red staining, and western blot analyses. Results: Glucose-induced oxidative stress led to increased production of H₂O₂, with negative impacts on cellular viability, ALP activity, and calcium deposition in HPDLCs. Furthermore, HPDLCs under glucose-induced oxidative stress showed induction of inflammatory molecules (intercellular adhesion molecule-1, vascular cell adhesion protein-1, tumor necrosis factor-alpha, interleukin-1-beta) and disturbances of osteogenic differentiation (bone morphogenetic protein-2, and -7, runt-related transcription factor-2), cementogenesis (cementum protein-1), and autophagy-related molecules (autophagy related 5, light chain 3 I/II, beclin-1). Phelligridin D restored all these molecules and maintained the function of HPDLCs even under glucose-induced oxidative stress. Conclusions: This study suggests that phelligridin D reduces the inflammation that results from glucose-induced oxidative stress and restores the function of HPDLCs (e.g., osteoblast differentiation) by upregulating autophagy.

• Molecules and Cells
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• v.27 no.3
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• pp.279-282
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• 2009

"Two-cysteine" peroxiredoxins are antioxidant enzymes that exert a cytoprotective effect in many models of oxidative stress. However, under highly oxidizing conditions they can be inactivated through hyperoxidation of their peroxidatic active site cysteine residue. Sulfiredoxin can reverse this hyperoxidation, thus reactivating peroxiredoxins. Here we review recent investigations that have shed further light on sulfiredoxin's role and regulation. Studies have revealed sulfiredoxin to be a dynamically regulated gene whose transcription is induced by a variety of signals and stimuli. Sulfiredoxin expression is regulated by the transcription factor AP-1, which mediates its up-regulation by synaptic activity in neurons, resulting in protection against oxidative stress. Furthermore, sulfiredoxin has been identified as a new member of the family of genes regulated by Nuclear factor erythroid 2-related factor (Nrf2) via a conserved cis-acting antioxidant response element (ARE). As such, sulfiredoxin is likely to contribute to the net antioxidative effect of small molecule activators of Nrf2. As discussed here, the proximal AP-1 site of the sulfiredoxin promoter is embedded within the ARE, as is common with Nrf2 target genes. Other recent studies have shown that sulfiredoxin induction via Nrf2 may form an important part of the protective response to oxidative stress in the lung, preventing peroxiredoxin hyperoxidation and, in certain cases, subsequent degradation. We illustrate here that sulfiredoxin can be rapidly induced in vivo by administration of CDDO-TFEA, a synthetic triterpenoid inducer of endogenous Nrf2, which may offer a way of reversing peroxiredoxin hyperoxidation in vivo following chronic or acute oxidative stress.

• Biomolecules & Therapeutics
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• v.22 no.4
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• pp.275-281
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• 2014

Autophagy is a series of catabolic process mediating the bulk degradation of intracellular proteins and organelles through formation of a double-membrane vesicle, known as an autophagosome, and fusing with lysosome. Autophagy plays an important role of death-survival decisions in neuronal cells, which may influence to several neurodegenerative disorders including Parkinson's disease. Chebulagic acid, the major constituent of Terminalia chebula and Phyllanthus emblica, is a benzopyran tannin compound with various kinds of beneficial effects. This study was performed to investigate the autophagy enhancing effect of chebulagic acid on human neuroblastoma SH-SY5Y cell lines. We determined the effect of chebulagic acid on expression levels of autophagosome marker proteins such as, DOR/TP53INP2, Golgi-associated ATPase Enhancer of 16 kDa (GATE 16) and Light chain 3 II (LC3 II), as well as those of its upstream pathway proteins, AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR) and Beclin-1. All of those proteins were modulated by chebulagic acid treatment in a way of enhancing the autophagy. Additionally in our study, chebulagic acid also showed a protective effect against 1-methyl-4-phenylpyridinium ($MPP^+$) - induced cytotoxicity which mimics the pathological symptom of Parkinson's disease. This effect seems partially mediated by enhanced autophagy which increased the degradation of aggregated or misfolded proteins from cells. This study suggests that chebulagic acid is an attractive candidate as an autophagy-enhancing agent and therefore, it may provide a promising strategy to prevent or cure the diseases caused by accumulation of abnormal proteins including Parkinson's disease.

• Korean Journal of Plant Tissue Culture
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• v.26 no.1
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• pp.15-19
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• 1999

For the induction of somatic embryogenic callus, the penduncle explants of Corydalis remota for peatinata were cultured on MS basal media supplemented with 2,4-D, kinetin and zeatin. The highest embryogenic callus formation was observed on the media containing 2.0 mg/L of 2,4-D and 2.0 mg/L of zeatin. The somatic embryogenesis on the media with 0.5 mg/L of cytokinin (zeatin or kinetin) were excellent under light condition, however somatic embryos abnormally developed into plantlets. Normal dicotyledonary plantlets were found on MS medium supplemented with 1.0 mg/L of zeatin. When MS medium with 2,4-D plus cytokinin and with BAP were used, the secondary somatic embryogenesis took place in root explants of the regenerants derived from in vitro somatic embryogenic callus.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.3
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• pp.1285-1292
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• 2016

Background: It is well established that mutations in the BRCA1 gene are a major risk factor for breast cancer. Induction of cancer cell death and inhibition of survival are the main principles of cancer therapy. In this context, autophagy may have dual roles in cancer, acting on the one hand as a tumor suppressor and on the other as a mechanism of cell survival that can promote the growth of established tumors. Therefore, understanding the role of autophagy in cancer treatment is critical. Moreover, defects in apoptosis, programmed cell death, may lead to increased resistance to chemotherapy. Purpose: The aim of the present study was to detect BRCA1 gene mutations in order to throw more light on their roles as risk factors for breast cancer in Egypt. Secondly the role of autophagy and apoptosis in determining response to a fluorouracil, doxorubicin, cyclophosphamide (FAC) regimen was investigated. Materials and Methods: Forty-five female breast cancer cases and thirty apparently healthy females were enrolled in the present study. Serum levels of autophagic biomarkers, Beclin 1 and LC3 as well as the serum levels of apoptosis biomarkers Bcl-2 and Caspase-3 were measured before and after chemotherapy. Results: BRCA1 mutations were found in 5 (16.7%) and 44 (99.8%) of the controls and cancer patients, the most frequent being 5382insC followed by C61G and 185 delAG. The results revealed that chemotherapy caused elevation in serum concentration levels of the autophagic biomarkers (Beclin 1 and LC3). This elevation was associated with a significant decrease in serum concentration levels of Bcl-2 and significant increase in caspase-3 concentration levels (apoptotic markers). Conclusions: The results of the present study indicate a very high level of BRCA mutations in breast cancer cases in Egypt and point to involvement of autophagic and apoptotic machinery activation in response to FAC chemotherapy.

• The Journal of Internal Korean Medicine
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• v.29 no.3
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• pp.582-594
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• 2008

Objective : The purpose of our study was to investigate the effect of JinlnWhaChul-tang-ga-wasong (JIN) on NDEA-induced liver tumorigenesis. Materials and Methods : We investigated the possible protective effects of Jininwhachul-tang-ga-wasong (JIN) as an anticancer against NDEA-induced liver injury in mice. Experimental mice were classified into 3 groups; normal, saline administered group (control group), and JIN extract (0.15g/kg/every other day) administered group (JIN group) after being injected with NDEA over 12 weeks. We examined the state of differentiation of these tumors and the effects of JIN after 6 weeks. To confirm the induction of apoptosis, the cells were analyzed by terminal deorynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay, acridine orange staining and flow cytometric analysis. To investigate inhibitory effect on the expression of COX-2 by JIN, we performed COX-2 immunohistochemistry and reverse transcription polymerase chain reaction analysis. Results : Body weights significantly decreased in the control and JIN groups compared with the normal group. The levels of cholesterol, hemoglobin and testosterone decreased in the control compared with the normal group. The level of estradiol significantly increased in the control compared with the normal group. The control group reacted with TUNEL assay more than the normal and JIN groups. Upon naked eye, light and electron microscopic examination, JIN improved the morphological and histopathological changes of the liver caused by NDEA-induced hepatic neoplasm. COX-2 immunoreactivity decreased in the JIN group compared with the control group, mRNA expression of the control group was greater than the normal and JIN groups. Conclusion : these results suggest the possibility that JIN may exert an anti-tumor effect on NDEA-induced liver tumorigenesis.

• The Journal of the Institute of Internet, Broadcasting and Communication
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• v.14 no.5
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• pp.95-102
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• 2014

In this paper, we propose the high speed PLC-based automatic control system for a smart LED streetlight. The proposed the automatic control system were constructed of a power line modem part and monitoring part, streetlight controller part for the high speed communication frequency band and streetlight ballasts characterization and real-time remote control using a high-speed PLC network, and it was designed to meet to lighting grades conditions of KS road lighting standards. The proposed automatic control system were easy monitoring of the power consumption using PC through to the comparison result of the existing streetlight system. As a result, it was confirmed to the possibility of efficient operation for the real-time monitoring and maintenance by induction of reasonable power consumption through to the LED streetlight state checking and remote-control. In addition, we proved to improvement of expected effects for the power cost savings, the energy efficiency, and streetlight differentiation and advanced.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.12
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• pp.5139-5145
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• 2016

There has been an increment in the number of studies focused on marine bioactive materials. Many peptides and other biomaterials with anticancer potential have been extracted from various marine animals. Artemia extracts have found uses in sun-light protection cosmetics and anti-aging products. However, contents of biochemical compounds in Artemia spp. and molecular mechanisms of have not been clearly studied in leukemic cells in vitro. In this work, we isolated and purified proteins of Artemia Urmiana. Six clear fractions (A-F) observed on DEAE-cellulose chromatography were assayed for effects on cell growth, differentiation and apoptosis using the human leukemic HL-60 cell line. Cell proliferation analysis by MTT and BrdU assays indicated that did not affect cells, growth. Cells treated with crude extract and fractions A, B and C, but not E and F (up to $100{\mu}g/mL$), exhibited increase of cell growth in a dose dependent manner. Stimulatory effects of fraction D were observed at concentrations of $10{\mu}g/mL$ and above. In nitro blue tetrazolium (NBT) reduction assays, treatment with $100{\mu}g/mL$ of fraction E or F for 96 hr increased the fraction of differentiated cells up to $14.8{\pm}3.56%$ and $16.5{\pm}2.08%$ respectively. Combination of those fractions with retinoic acid had significant synergistic effects on the differentiation of cells ($56.8{\pm}3.7%$ and $67.4{\pm}4.2%$, $p{\leq}0.01$). Annexin-V FITC staining for apoptosis and flow cytometric assays indicated induction of apoptosis by fractions E and F up to 23.8 and 31.8% of cells.