• Tuberculosis and Respiratory Diseases
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• v.65 no.6
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• pp.476-486
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• 2008

Background: TRAIL (TNF-related apoptosis inducing ligand) is a newly identified member of the TNF gene family which appears to have tumor-selective cytotoxicity due to the distinct decoy receptor system. TRAIL has direct access to caspase machinery and induces apoptosis regardless of p53 phenotype. Therefore, TRAIL has a therapeutic potential in lung cancer which frequently harbors p53 mutation in more than 50% of cases. However, it was shown that TRAIL also could activates $NF-{\kappa}B$ in some cell lines which might inhibit TRAIL-induced apoptosis. This study was designed to investigate whether TRAIL can activate $NF-{\kappa}B$ in lung cancer cell lines relatively resistant to TRAIL-induced apoptosis and inhibition of $NF-{\kappa}B$ activation using proteasome inhibitor MG132 which blocks $I{\kappa}B{\alpha}$ degradation can sensitize lung cancer cells to TRAIL-induced apoptosis. Methods: A549 (wt p53) and NCI-H1299 (null p53) lung cancer cells were used and cell viability test was done by MTT assay. Apoptosis was confirmed with Annexin V assay followed by FACS analysis. To study $NF-{\kappa}B$-dependent transcriptional activation, a luciferase reporter gene assay was used after making A549 and NCI-H1299 cells stably transfected with IgG ${\kappa}-NF-{\kappa}B$ luciferase construct. To investigate DNA binding of $NF-{\kappa}B$ activated by TRAIL, electromobility shift assay was used and supershift assay was done using anti-p65 antibody. Western blot was done for the study of $I{\kappa}B{\alpha}$ degradation. Results: A549 and NCI-H1299 cells were relatively resistant to TRAIL-induced apoptosis showing only 20~30% cell death even at the concentration 100 ng/ml, but MG132 ($3{\mu}M$) pre-treatment 1 hour prior to TRAIL addition greatly increased cell death more than 80%. Luciferase assay showed TRAIL-induced $NF-{\kappa}B$ transcriptional activity in both cell lines. Electromobility shift assay demonstrated DNA binding complex of $NF-{\kappa}B$ activated by TRAIL and supershift with p65 antibody. $I{\kappa}B{\alpha}$ degradation was proven by western blot. MG132 completely blocked both TRAIL-induced $NF-{\kappa}B$ dependent luciferase activity and DNA binding of $NF-{\kappa}B$. Conclusion: This results suggest that inhibition of $NF-{\kappa}B$ can be a potentially useful strategy to enhance TRAIL-induced tumor cell killing in lung cancer.

• Korean Journal of Soil Science and Fertilizer
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• v.44 no.3
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• pp.465-472
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• 2011

To investigate the effect of inorganic ($GeO_2$) and organic (Ge-132) germanium treatment on Brasica juncea C. plant, growth characteristics and Ge contents were examined with various inorganic or organic germanium treatments (0, 5, 10, 25, 50, 75 and $100mg\;L^{-1}$), respectively. Brasica juncea C. growth did not much inhibited until Ge $10mg\;L^{-1}$ concentration under both Ge-132 and $GeO_2$ treatments as compared to control. On the other hand, at Ge concentration higher than $25mg\;L^{-1}$ concentration, Brasica juncea C. growth was inhibited under both Ge-132 and $GeO_2$ treatments. Under treatment of $GeO_2$, length of root and shoot slightly increased until $5mg\;L^{-1}$ concentration and dry weight slightly increased until $10mg\;L^{-1}$ concentration. Under treatment of Ge-132, length of root and shoot slightly increased until $10mg\;L^{-1}$ concentration and dry weight slightly increased until $25mg\;L^{-1}$ concentration. Total Ge contents in Brasica juncea C. early seedlings with $GeO_2$ treatment were a bit higher than those with Ge-132 treatment. Germanium was primarily accumulated in the roots (77%) with organic Ge (Ge-132) treatments, whereas Ge was primarily accumulated in the leaf (70%, respectively) with $GeO_2$ treatments. The Ge uptake rates in inorganic Ge treatments were slightly high than those in organic Ge treatments. Under inorganic Ge treatment with $2.5mg\;L^{-1}$, about 3% of Ge was accumulated into plant and distribution in leaf and root was 84.8% and 15.2%, respectively. Under organic Ge treatment with $2.5mg\;L^{-1}$, about 2.6% of Ge was accumulated into plant and distribution in leaf and root was 66.4% and 33.6%, respectively.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.9
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• pp.1061-1070
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• 2017

This study examined the physicochemical properties and protective effects of Corni fructus treated with pressurized-steam (through $121^{\circ}C$, $1.2kgf/cm^2$, 0.5 h, 1 h, 2 h, and 3 h) against $H_2O_2$-induced cytotoxicity on L132 cells. The color values of the untreated Corni fructus powder were higher than those of Corni fructus after the pressurized-steam treatment (PSC), and those of PSC improved with a decrease in treatment time. At the observation by pressurized-steam treatment for more than 2 h, the color was changed to black, and its gloss was lost. The major constituents in PSC (2 hours) were the total sugar (468.53 mg/g), reducing sugar (385.55 mg/g), and total phenol (37.32 mg/g), respectively. The main components in the free sugars of PSC (2 h) were fructose, glucose, and sucrose, at 207.72 mg/g, 219.40 mg/g, and 4.31 mg/g, respectively. The gallic acid in the phenol compounds and 5-(hydroxymethyl) furfural in the furan compounds of PSC (2 h) improved with increasing treatment time. The main components in iridoid glycoside of PSC (2 h) were morroniside, loganin, and lognic acid, which improved with decreasing treatment time. The L132 cell growth inhibition activities of all the extracts were significantly higher than that of the control. The protective effects against the $H_2O_2$-induced cytotoxicity on L132 cells of PSC (2 h) was 102.82% (at $1,000{\mu}g/mL$) higher than those of the other extracts. This suggests that Corni fructus by PSC is useful for functional food materials in the food industry.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1994.04a
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• pp.320-320
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• 1994

Carboxyethylgermanium sesquioxide(Ge-132)를 투여용량(300,600, 900mg/kg)과 투여일을 변화시켜 정상마우스와 cyclophosphamide(CY)로 처리한 마우스에 경구투여한 후, Ge-132가 CY 에 의해 변화된 마우스의 면역기능에 미치는 효과를 실험하였다. SRBC 항원 주사전, 동시 또는 후에 Ge-132를 투여시 SRBC에 대한 적혈구 응집소가와 비장세포의 용혈반 형성세포(PFC)수가 항원 주사일과 관계없이 용량의존적으로 증가되어 체액성 면역반응을 강화시켰으며, 마크로파지의 탐식능도 항진시켰다. 그러나 DNFB에 대한 접촉성 지연형 과민반응은 DNFB 감작일과 투여용량에 관계없이 Ge-132투여로 억제되었다. CY를 투여한 마우스에 Ge-132를 병용 투여한 군이 CY 단독 투여군에 비하여 적혈구 응집소가와 PFC수 및 혈중 탄소입자의 제거율이 현저하게 증가되어, CY로 억제된 체액성 면역반응과 마크로파지의 탐식능이 항진된 것으로 나타났다. DNFB 감작 전 CY 투여로 증폭된 접촉성 지연형 과민반응이 Ge-132 병용투여로 감소되어 CY로 유도된 면역독성 반응에 대한 Ge-132의 저지효과를 시사해 주었다.

• Proceedings of the Korean Society of Life Science Conference
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• 2008.10a
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• pp.88.1-88.1
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• 2008

• Proceedings of the Korean Society of Life Science Conference
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• 2008.10a
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• pp.88.2-88.2
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• 2008

• Journal of Magnetics
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• v.7 no.4
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• pp.132-137
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• 2002

The electronic structures and magnetism of the non-oxide perovskite MgCFe$_3$(001) surface were investigated by using the all-electron full-potential linearized augmented plane wave (FLAPW) method within the generalized gradient approximation (GGA). We considered both of the MgFe terminated (MgFe-Term) and the CFe terminated (CFe-Term) surfaces. We found that the minority spin d-bands of Fe(S) of the MgFe-Term are strongly localized and Fermi level (EF) lies just below the sharp peak of the minority spin d-band of Fe(S), while the minority spin d-bands of Fe(S) of the CFe-Term are not localized much and Fermi level (E$_F$) lies in the middle of two peaks of the minority spins. The majority Fe(S) d-band width of MgFe- Term is narrower than that of the CFe-Term. It is found that the magnetic moment of Fe(S) of the MgFe- Term is 2.51 ${\mu}$$_B$, which is much larger than that of 1.97 ${\mu}$$_B$ of the CFe-Term.

• YAKHAK HOEJI
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• v.35 no.2
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• pp.99-110
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• 1991

This study was initiated to investigate the effects of organic germanium on cadmium and mercury intoxication. The effect was determined by the metallothionein induction in liver and kidney. Male rats (Sprague-Dawley) were treated with CdCI$_{2}$ (2mg/kg), HgCI$_{2}$ (1 mg/kg) and organic germanium (GE-132) (100 mg/kg) in single and in combination via intraperitoneal injection or intragastric administration every other days for 17 days. Experimental animals were sacrificed after 7, 12 and 17 days treatment. The serum transaminase activities (SGOT, SGPT), concentration of metal and metallothionein, metal-binding capacity of metallothionein in liver and kidney were determined and pathomorphological observations were undertaken. The combined treatment of GE-132 and CdCI$_{2}$ significantly decreased the increment of serum transaminase activities in rats treated with CdCI$_{2}$ only, but the combined treatment of GE-132 and HgCI$_{2}$ did not affect to activities of transaminases induced by mercury only. The concentration of metals (Cd and Hg) except Ge in the liver and kidney of rats increased with the time of treatment. Mercury concentration in kidney of rat treated with HgCI$_{2}$ only was significantly higher than the combined treatment of GE-132 and HgCI$_{2}$. The combined treatment of GE-132 and CdCI$_{2}$ significantly increased the concentration of metallothionein in liver compared to the CdCI$_{2}$ only, although the concentration of cadmium in liver were not significantly different between two groups. This indicates that GE-132 decreased toxicity of cadmium in liver by promoting metallothionein induction. There were no significant differences in metallothionein concentration in liver and kidney of rats between the combined treatment of GE-132 and HgCI$_{2}$ and HgCI$_{2}$ only. Metal-binding capacity of metallothionein varied with each time intervals in liver and kidney of metals treated rats except the liver of the combined treatment of GE-132 and CdCI$_{2}$. This finding explains the concentration of metallothionein in liver keeps abreast with the concention of metal. Furthermore, the combined treatment of GE-132and CdCl$_{2}$ revealed pathologically less changes in liver tissue than CdCl$_{2}$ only; the damages of liver cell, such as lobular necrosis and portal inflammation, were relieved and appeared more later. From the above results, organic germanium is considered to have some beneficial effect on the protection of liver from the cadmium intoxication.

• Proceedings of the Korean Magnestics Society Conference
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• 2007.05a
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• pp.132.1-132.1
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• 2007

• BMB Reports
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• v.49 no.5
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• pp.270-275
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• 2016

The Ubiquitin proteasome system (UPS) plays roles in protein degradation, cell cycle control, and growth and inflammatory cell signaling. Dysfunction of UPS in cardiac diseases has been seen in many studies. Cholesterol acts as an inducer of cardiac hypertrophy. In this study, the effect of proteasome inhibitors on the cholesterol-induced hypertrophic growth in H9c2 cells is examined in order to observe whether UPS is involved in cardiac hypertrophy. The treatment of proteasome inhibitors MG132 and Bortezomib markedly reduced cellular surface area and mRNA expression of β-MHC in cholesterol-induced cardiac hypertrophy. In addition, activated AKT and ERK were significantly attenuated by MG132 and Bortezomib in cholesterol-induced cardiac hypertrophy. We demonstrated that cholesterol-induced cardiac hypertrophy was suppressed by proteasome inhibitors. Thus, regulatory mechanism of cholesterol-induced cardiac hypertrophy by proteasome inhibitors may provide a new therapeutic strategy to prevent the progression of heart failure.