• Korean Journal of Agricultural Science
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• v.24 no.2
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• pp.132-137
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• 1997

Effective storage facilities are required to stabilize the price of agricultural and marine products to preserve their qualities due to the big fluctuation of shrimp price in Korea. It is easy to make the cave because of good conditions of the land configuration, soil and convenient transportation. The cave storage can save the cost about 40% in building site and equipment, and about 50% in maintenance comparing to existing low temperature storage facilities. The cave storage provide to improve the quality of their stored products with the low heat conductivity, the constant temperature and humidity year round. Therefore, more low temperature storage facilities are required because the items are expanded from potatoes, sweet potatoes, onions, garlics, apples and chestnuts to tangerines, grapes, cabbages, radishes, and wet ginsengs. The demands of the low temperature storage facilities can be substituted into the cave storage facilities. Thus, studies are conducted to observe the changes of the components of the pure and the seasoned salted shrimps with fermentation period during stored at room temperature in cave and to establish the storing at underground facilities to produce high quality salted fish to make profit.

• Korean Journal of Food Science and Technology
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• v.37 no.5
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• pp.822-826
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• 2005

Effect of Cheonnyuncho extract on the liver injury of rats treated carbon tetrachloride $(CCl_4)$ was studied. Cheonnyuncho extract was administerd at dose of 0.5 and 1 g/kg/day, p.o. for 2 weeks. $CCl_4$ was treated at dose of $0.5\;mL/kg$, i.p. 3 hours later from the last pretreatment of Cheonnyuncho extract. Administration of Cheonnyuncho extract at a dose of 1 g/kg decreased serum AST, ALT and ALP activities by 36, 41, and 22% respectively compared to $CCl_4$ treatment group. Increased lipid peroxidation and decreased SOD and GST activities were also recovered by pretreatment of Chonnyuncho extract in liver of rats. These results suggest that Cheonnyuncho extract has hepatoprotective effect against liver injury.

• Journal of Pharmacopuncture
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• v.7 no.1 s.12
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• pp.87-100
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• 2004

Objective : This research was performed to investigate the effect of herbal acupuncture(Atratylodes japonica, Coix lachrymajobi, Ephedra sinica, Atratylodes japonica mixed with Coix lachrymajobi and Ephedra sinica mixed with Green tea) at Pungnyung(ST40) and Umnungchon(SP9) on weight gain, food intake, food efficiency, serum of lipid concentrations, liver function and HDL to total cholesterol ratio of rats fed high fat diet for 5weeks. Method : Experimental groups were divided into normal group(Normal), high fat diet group(Control), high fat diet and Atractylodes japonica-herbal acupuncture group(AJ), high fat diet and Coix lachrymajobi-herbal acupuncture group(CL), high fat diet and Ephedra sinica-herbaI acupuncture group(ES), high fat diet and Atractylodes japonica+Coix lachrymajobi-herbal acupuncture group(AJ+CL), Ephedra sinica+Green tea-herbal acupuncture group(ES+GT). Herbal acupuncture was bilaterally treated at the level of 132.5mg/kg body weight per 2day. Results : Body weight and food efficiency were decreased in AJ, ES, AJ+CL, ES+GT. The level of serum total cholesterol, triglyceride and free fatty acid were increased in AJ, ES, ES+GT. That of serum HDL-cholesterol was increased in AJ. The change of food intake, the level of serum phospholipid and ALP were not significant. The HDL to Total cholesterol ratio was increased in AJ and ES. Conclusion : Atractylodes japonica-herbal acupuncture in ST40 SP9 is effective on Body weight, food efficiency ratio, the level of serum lipid, protection of liver function and prevention cardiovascular risk by obesity induced by high fat diet. Herbal acupuncture mixed Ephedra sinica with Green tea can control the body weight, food efficiency ratio and the level of serum lipid.

• Korean Journal of Medicinal Crop Science
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• v.25 no.5
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• pp.328-334
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• 2017

Background: In this study, we evaluated the anti-cancer activity and potential molecular mechanism of 70% ethanol extracts of the root of Aralia cordata var. continentalis (Kitagawa) Y. C. Chu (RAc-E70) against human colorectal cancer cells. Methods and Results: RAc-E70 suppressed the proliferation of the human colorectal cancer cell lines, HCT116 and SW480. Although RAc-E70 reduction cyclin D1 expression at the protein and mRNA levels, RAc-E70-induced reduction in cyclin D1 protein level occurred more dramatically than that of cyclin D1 mRNA. The RAc-E70-induced downregulation of cyclin D1 expression was attenuated in the presence of MG132. Additionally, RAc-E70 reduced HA-cyclin D1 levels in HCT116 cells transfected with HA-tagged wild type-cyclin D1 expression vector. RAc-E70-mediated cyclin D1 degradation was blocked in the presence of LiCl, a $GSK3{\beta}$ inhibitorbut, but not PD98059, an ERK1/2 inhibitor and SB203580, a p38 inhibitor. Furthermore, RAc-E70 phosphorylated cyclin D1 at threonine-286 (T286), and LiCl-induced $GSK3{\beta}$ inhibition reduced the RAc-E70-mediated phosphorylation of cyclin D1 at T286. Conclusions: Our results suggested that RAc-E70 may downregulate cyclin D1 expression as a potential anti-cancer target through $GSK3{\beta}$-dependent cyclin D1 degradation. Based on these findings, RAc-E70 maybe a potential candidate for the development of chemopreventive or therapeutic agents for human colorectal cancer.

• Journal of the Korean Society of Food Science and Nutrition
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• v.22 no.2
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• pp.132-137
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• 1993

These studies were carried out to investigate the effects of ascorbate and $\alpha$-tocopherol administration on the biochemical parameters of liver function and hydroperoxidation in liver of chronically ethanol-treated rats. Forty healthy Sprague-Dawley (SD) rats weighing about 120g were used for this experiment and divided into the following 5 groups: control group (CON), ethanol control group (ECON), ascorbate treated group (EASC), $\alpha$-tocopherol treated group (ETOC) and ascorbate.$\alpha$-tocopherol mixture treated group(EASC + ETOC). Ethanol was administered orally by 5ml per kg, body weight per day for 8weeks. Antioxidants treated groups were administered orally by 5mg per kg body weight per day in saline solution for 3 weeks. Lipid hydroperoxides were analyzed by using chemiluminescense-high performance liquid chromatography (CL-HPLC) method phosphatidylcholine hydroperoxide value (PCOOH) in liver tissues. Ethanol treatment significantly (p<0.05) resulted in an increase in GPT and GOT activities and liver hydroperoxide values comparing with the untreated control, while administration of $\alpha$-tocopherol and ascorbate+$\alpha$-tocopherol to the chronically ethanol-treated rats significantly (p<0.001) decreased GPT and GOT activities and liver hydroperoxide value. These results indicate that dietary $\alpha$-tocopherol and $\alpha$-tocopherol combined with ascorbate administration may inhibit the formation of liver lipid hydroperoxidation in vivo and were very effective in recovering the liver function in chronically ethanol-treated rats.

• Korean Journal of Plant Resources
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• v.32 no.5
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• pp.442-447
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• 2019

In this study, we evaluated the effect of Rodgersia podophylla leave extracts (RPL) on ${\beta}-catenin$ level in human cancer cells. RPL dose-dependently inhibited cell proliferation in SW480, A549, MDA-MB-231, PC-3 and AsPC-1 cells. RPL dramatically decreased ${\beta}-catenin$ protein level in all cancer cells. However, decreased level of ${\beta}-catenin$ mRNA expression was observed in A549 and AsPC-1 cells. In addition, RPL dramatically attenuated cyclin D1 mRNA expression in all cancer cells. MG132 decreased the downregulation of ${\beta}-catenin$ protein level induced by RPL in all cancer cells, while RPL-induced downregulation of ${\beta}-catenin$ was inhibited by the inhibition of $GSK-3{\beta}$ by LiCl in MDA-MB-231 cells. RPL phosphorylated ${\beta}-catenin$ and $GSK-3{\beta}$. In addition, the inhibition of $GSK-3{\beta}$ by LiCl attenuated RPL-induced ${\beta}-catenin$ phosphorylation. Based on these findings, RPL may be a potential candidate for the development of chemopreventive or therapeutic agents for human cancer.

• Molecules and Cells
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• v.41 no.12
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• pp.1008-1015
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• 2018

$I{\kappa}B$, a cytoplasmic inhibitor of nuclear factor-${\kappa}B$ ($NF-{\kappa}B$), is reportedly degraded via the proteasome. However, we recently found that long-term incubation with proteasome inhibitors (PIs) such as PS-341 or MG132 induces $I{\kappa}B{\alpha}$ degradation via an alternative pathway, lysosome, which results in $NF-{\kappa}B$ activation and confers resistance to PI-induced lung cancer cell death. To enhance the anti-cancer efficacy of PIs, elucidation of the regulatory mechanism of PI-induced $I{\kappa}B{\alpha}$ degradation is necessary. Here, we demonstrated that PI up-regulates nuclear factor (erythroid-derived 2)-like 2 (Nrf2) via both de novo protein synthesis and Kelch-like ECH-associated protein 1 (KEAP1) degradation, which is responsible for $I{\kappa}B{\alpha}$ degradation via macroautophagy activation. PIs increased the protein level of light chain 3B (LC3B, macroautophagy marker), but not lysosome-associated membrane protein 2a (Lamp2a, the receptor for chaperone-mediated autophagy) in NCI-H157 and A549 lung cancer cells. Pretreatment with macroautophagy inhibitor or knock-down of LC3B blocked PI-induced $I{\kappa}B{\alpha}$ degradation. PIs up-regulated Nrf2 by increasing its transcription and mediating degradation of KEAP1 (cytoplasmic inhibitor of Nrf2). Overexpression of dominant-negative Nrf2, which lacks an N-terminal transactivating domain, or knock-down of Nrf2 suppressed PI-induced LC3B protein expression and subsequent $I{\kappa}B{\alpha}$ degradation. Thus, blocking of the Nrf2 pathway enhanced PI-induced cell death. These findings suggest that Nrf2-driven induction of LC3B plays an essential role in PI-induced activation of the $I{\kappa}B$/$NF-{\kappa}B$ pathway, which attenuates the anti-tumor efficacy of PIs.

• Korean Journal of Plant Resources
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• v.32 no.2
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• pp.153-159
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• 2019

In this study, we evaluated the effect of branch (STB) and leave (STL) extracts from Sageretia thea on ${\beta}-catenin$ level in human colorecal cancer cells, SW480 and lung cancer cells, A549. STB and STL dose-dependently suppressed the growth of SW480 and A549 cells. STB and STL decreased ${\beta}-catenin$ level in both protein and mRNA level. MG132 decreased the downregulation of ${\beta}-catenin$ protein level induced by STB and STL. However, the inhibition of $GSK3{\beta}$ by LiCl or ROS scavenging by NAC did not block the reduction of ${\beta}-catenin$ protein by STB and STL. Our results suggested that STB and STL may downregulate ${\beta}-catenin$ protein level independent on $GSK3{\beta}$ and ROS. Based on these findings, STB and STL may be a potential candidate for the development of chemopreventive or therapeutic agents for human colorectal cancer and lung cancer.

• Korean Journal of Plant Resources
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• v.32 no.2
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• pp.109-115
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• 2019

In this study, we evaluated the anti-cancer activity and potential molecular mechanism of 70% ethanol extracts of branches from Taxillus yadoriki parasitic to Neolitsea sericea (TN-NS-B) against human lung cancer cells, A549. TY-NS-B dose-dependently suppressed the growth of A549 cells. TY-NS-B decreased ${\beta}$-catenin protein level, but not mRNA level in A549 cells. The downregulation of ${\beta}$-catenin protein level by TY-NS-B was attenuated in the presence of MG132. Although TY-NS-B phosphorylated ${\beta}$-catenin protein, the inhibition of $GSK3{\beta}$ by LiCl did not blocked the reduction of ${\beta}$-catenin by TY-NS-B. In addition, TY-NS-B decreased ${\beta}$-catenin protein in A549 cells transfected with Flag-tagged wild type ${\beta}$-catenin or Flag-tagged S33/S37/T41 mutant ${\beta}$-catenin construct. Our results suggested that TN-NS-B may downregulate ${\beta}$-catenin protein level independent on $GSK3{\beta}$-induced ${\beta}$-catenin phosphorylation. Based on these findings, TY-NS-B may be a potential candidate for the development of chemopreventive or therapeutic agents for human lung cancer.

• Journal of Korean Neurosurgical Society
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• v.65 no.6
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• pp.790-800
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• 2022

Objective : EID3 (EP300-interacting inhibitor of differentiation) was identified as a novel member of EID family and plays a pivotal role in colorectal cancer development. However, its role in glioma remained elusive. In current study, we identified EID3 as a novel oncogenic molecule in human glioma and is critical for glioma cell survival, proliferation and invasion. Methods : A total of five patients with glioma were recruited in present study and fresh glioma samples were removed from patients. Four weeks old male non-obese diabetic severe combined immune deficiency (NOD/SCID) mice were used as transplant recipient models. The subcutaneous tumor size was calculated and recorded every week with vernier caliper. EID3 and AMP-activated protein kinase α1 (AMPKα1) expression levels were confirmed by real-time polymerase chain reaction and Western blot assays. Colony formation assays were performed to evaluate cell proliferation. Methyl thiazolyl tetrazolium (MTT) assays were performed for cell viability assessment. Trypan blue staining approach was applied for cell death assessment. Cell Apoptosis DNA ELISA Detection Kit was used for apoptosis assessment. Results : EID3 was preferentially expressed in glioma tissues/cells, while undetectable in astrocytes, neuronal cells, or normal brain tissues. EID3 knocking down significantly hindered glioma cell proliferation and invasion, as well as induced reduction of cell viability, apoptosis and cell death. EID3 knocking down also greatly inhibited tumor growth in SCID mice. Knocking down of AMPKα1 could effectively rescue glioma cells from apoptosis and cell death caused by EID3 absence, indicating that AMPKα1 acted as a key downstream regulator of EID3 and mediated suppression effects caused by EID3 knocking down inhibition. These findings were confirmed in glioma cells generated patient-derived xenograft models. AMPKα1 protein levels were affected by MG132 treatment in glioma, which suggested EID3 might down regulate AMPKα1 through protein degradation. Conclusion : Collectively, our study demonstrated that EID3 promoted glioma cell proliferation and survival by inhibiting AMPKα1 expression. Targeting EID3 might represent a promising strategy for treating glioma.