• The Korean Journal of Physiology and Pharmacology
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• v.21 no.5
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• pp.565-565
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• 2017

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.174.2-175
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• 2002

• Biomolecules & Therapeutics
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• v.30 no.4
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• pp.389-389
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• 2022

• BMB Reports
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• v.45 no.8
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• pp.470-475
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• 2012

Protein arginine methyltransferase 1 (PRMT1), a type-I arginine methyltransferase, has been implicated in diverse cellular events. We have focused on the role of PRMT1 in gliomagenesis. In this study, we showed that PRMT1 expression was up-regulated in glioma tissues and cell lines compared with normal brain tissues. The knock-down of PRMT1 resulted in an arrest in the G1-S phase of the cell cycle, proliferation inhibition and apoptosis induction in four glioma cell lines (T98G, U87MG, U251, and A172). Moreover, an in vivo study confirmed that the tumor growth in nude mouse xenografts was significantly decreased in the RNAi-PRMT1 group. Additionally, we found that the level of the asymmetric dimethylated modification of H4R3, a substrate of PRMT1, was higher in glioma cells than in normal brain tissues and decreased after PRMT1 knock-down. Our data suggest a potential role for PRMT1 as a novel biomarker of and therapeutic target in gliomas.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.223.2-224
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• 2003

Glial cell-derived neurotrophic factor (GDNF) is a potent neurotrophic factor that enhances survival of midbrain doparminergic neuron. GDNF and its receptors are widely distributed in brain and are believed to be involved in the control of neuron survival and differentiation. GDNF increased proliferation and migration of Hs683 human giloma and C6 rat giloma cells in a dose-dependent manner. (omitted)

• Journal of Physiology & Pathology in Korean Medicine
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• v.24 no.3
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• pp.401-409
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• 2010

This study was designed to investigate the effects of BojungIkkiTang-Gamybang freeze dried powder (BITG) on proliferauion, protective of cell death induced by chemicals such as paraquat, hydrogen peroxide etc and anti-oxidative effects in C6 glioma cells. In our results, BITC accelerated proliferation rates of C6 cells in vitro. In addition, protective effects on cell death induced by paraquat and hydrogen peroxide. And, BITC did not have effects on SOD and total glutathione activities, but decresed malone dialdehyde activity. In conclusion, these results suggest the possibility of BojungIkkiTang-Gamybang to protect brain cell or neuronal cell from damage induced by oxidative stress. And also suggest that related mechanisms are involved in malone dialdehyde activity.

• The Journal of Internal Korean Medicine
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• v.22 no.2
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• pp.183-191
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• 2001

신경교세포에서 황금추출물이 반응성 산소기에 의한 세포 사망을 방지할 수 있는지를 확인하기 위하여 사람의 glioama 세포주인 A172 세포를 사용하여 $H_2O_2$의 독성작용에 대한 영향을 조사하였다. 세포 사망 정도는 tryptan blue exclusion과 MTT reduction assay로 평가하였다. $H_2O_2$는 세포 사망을 유도하였으며 또한 세포내 ATP 함량을 감소시켰으며, 이러한 효과는 황금 추출물에 의해 방지되었으며 그 효과는 농도 의존적으로 나타났다. $H_2O_2$에 의한 세포 사망은 잘 알려진 flavonoid인 quercetin과 철착염제인 phenanthroline에 의해 방지되었으나, 항산화제인 DPPD나 Trolox에 의해서는 영향을 받지 않았다. $H_2O_2$는 poly (ADP-ribose) polymerase를 활성화시켰으며, 이러한 효과는 황금, quercetin 및 phenanthroline에 의해 억제되었다. 황금 추출물은 유기산화제인 t-buthyhydroperoxide 및 중금속인 수은에 의한 세포 사망을 방지하였다. 이러한 실험 결과는 황금 추출물이 $H_2O_2$에 의한 세포 사망을 방지하며 그 효과는 황금의 flavonoid 성분이 철과 결합하여 $H_2O_2$로부터 hydroxy radical의 생성을 억제함으로써 나타나는 것으로 추측된다.

• Toxicological Research
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• v.20 no.1
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• pp.63-69
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• 2004

Casapse-3 protease is known as a key role of apoptotic enzyme, and caspase-3 activity is a central event that occurs upstream of DNA fragmentation during apoptosis. This study demonstrates that chitosan pretreatment inhibits cadmium-induced apoptosis by attenuating the activity of caspase-3. We also analyzed the protective effect of chitosan on DNA fragmentation induced by cadmium. Cadmium toxicity was examined by DNA fragmentation and nuclear condensation with Hoechst stain. Caspase-3 activities were increased cadmium treated group for 3 hours compared with control. When chitosan (150 mg/ml) was pretreated at 30 min before cadmium treatment, cadmium cytotoxicity was suppressed in a dose-dependent manner evaluated by DNA fragmentation and caspase activity. From these results, it is suggest that the protective effect of chitosan pretreatment against cadmium-induced cytotoxicity is mediated through inhibition of caspase-3 protease activation and DNA fragmentation.

• The Journal of Korean Medicine
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• v.26 no.2 s.62
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• pp.1-12
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• 2005

Objectives: Malignant gliomas are often treated with cisplatin (cis-diamminedichloroplatinum(II), CDDP) and radiation but results remain unsatisfactory. Since malignant glioma displays moderate resistance to conventional therapy, a new treatment modality is needed to improve the outcome of patients with these tumors. The aim of this study was to investigate the effects of the combined use of Jongjihwan(JJH) and cisplatin(CDDP) on cultured malignant glioma cells, A172. Methodss & Results: The combined use of cisplatin and Jeongjihwan had synergistic effects on Al72 cells during 24 hr-incubation, This treatment resulted in a decrease of cell viability, Which was revealed as apoptosis Characterized by activation of caspase-3 protease as well as cleavage of poly ADP-ribose polymerase (PARP) with change of mitochondria membrane potential transition. The expression of members of the Bcl-2 protein family was modulated during co-treatment with Jeongjihwan and cisplatin. Activation of caspase-3 and mitochondrial alterations were central to co-treatment with Jeongjihwan and cisplatin-induced apoptosis. Conclusions: We conclude that co-treatment with Jeongjihwan and cisplatin-induced activation of the mitochondrial pathway enables cell death. Also, we suggest the combined theory of JJH and cisplatin could be a useful method for glioblastoma.

• YAKHAK HOEJI
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• v.60 no.2
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• pp.92-99
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• 2016

Parkinson's disease (PD) is one of the representative neurodegenerative movement disorders with the selective loss of dopaminergic neurons in the substantia nigra. 6-Hydroxydopamine (6-OHDA) is widely used as an experimental model system to mimic PD and has been reported to cause neuronal cell death via oxidative and/or nitrosative stress. Therefore, daily intake of dietary or medicinal plants which fortifies cellular antioxidant capacity can exert neuroprotective effects in PD. In the present study, we have investigated the protective effect of Korean red ginseng (KRG) against 6-OHDA-induced nitrosative death in C6 glioma cells. Treatment of C6 cells with 6-OHDA decreased cell viability and increased expression of inducible nitric oxide synthase, production of nitric oxide as well as peroxynitrite, and formation of nitrotyrosine. 6-OHDA led to apoptotic cell death as determined by decreased Bcl-2/Bax, phosphorylation of JNK, activation of caspase-3, and cleavage of PARP. Conversely, pretreatment of C6 cells with KRG attenuated 6-ODHA-induced cytotoxicity, apoptosis, and nitrosative damages. To further elucidate the molecular mechanism of KRG protection against 6-OHDA-induced nitrosative cell death, we have focused on the cellular self-defense molecules against exogenous noxious stimuli. KRG treatment up-regulated heme oxygenase-1 (HO-1), a key antioxidant enzyme essential for cellular defense against oxidative and/or nitrosative stress via activation of Nrf2. Taken together, these findings suggest KRG may have preventive and/or therapeutic potentials for the management of PD.