• Korean Journal of Clinical Laboratory Science
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• v.50 no.2
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• pp.170-176
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• 2018

This study examined the antioxidative effects of Cornis fructus (CF) extract on cultured C6 glioma cells. For this purpose, cytotoxicity analysis of chromium trioxide ($CrO_3$) was performed and the protective effects of the CF extract on $CrO_3$-induced cytotoxicity was examined after the C6 glioma cells were cultured for 48 hours. The antioxidative effects, such as electron donating activity (EDA) and lactate dehydrogenase (LDH) activity were also analyzed. In this study, $CrO_3$ decreased the cell viability in a dose dependent manner. The $XTT_{50}$ value was determined to be $33{\mu}M$ after the cells were treated for 48 hours at a concentrations of $20{\sim}40{\mu}M$ $CrO_3$. The catalase (CAT) antioxidant increased significantly the cell viability that had been decreased by $CrO_3$-induced cytotoxicity. Regarding the protective effect of the CF extract, the cell viability of the CF extract was increased significantly compared to that of $CrO_3$ only. In addition, the CF extract showed antioxidative effects, such as EDA and an inhibitory effect on the LDH activity. These findings suggest that the cytotoxicity of $CrO_3$ is correlated with oxidative stress, and the CF extract effectively prevented $CrO_3$-induced cytotoxicity through the antioxidative effects. In conclusion, natural products, such as the CF extract may be a useful therapeutic agent for the prevention or treatment of toxicity induced by heavy metals via oxidative stress.

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

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.6
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• pp.1292-1298
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• 2009

Sipjeon-Daebo-Tang (SDT) is indicated for deficiency syndrome of both gi and blood, marked by pale or sallow complexion, dizziness, lassitude, shortness of breath, dislike for talking, poor appetite, pale tongue with thin whitish fur, thready and weak pulse. Gami-Sipjeon-Daebo-Tang(GSDT) is composed of 10 herbs within SDT and Cervi Pantotrichum Cornu (CPC). CPC can noursh kidney-yang, promote the production of the essence and blood, strengthen tendons and bones. Recently SDT is known as anti-cancer drug. Especially CPC is reported to have anti-oxidative action. For these reasons, we investigated the protective effects on cell death induced by chemicals such as paraquat, hydrogen peroxide and anti-oxidative effects in C6 glioma cells. In our results, GSDT accelerated proliferation rates of C6 cells in vitro. In addition, protective effects on cell death induced by hydrogen peroxide and rotenone. In addition, SOD activities were increased by treatment with both SDT and GSDT. In conclusion, these results suggest the possibility of GSDT to protect brain cell or neuronal cell from damage induced by oxidative stress. And also suggest that related mechanisms are involved in SOD activities.

• Biomolecules & Therapeutics
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• v.26 no.2
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• pp.175-181
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• 2018

Carbon monoxide (CO) is well-known as toxic gas and intrinsic signaling molecule such as neurotransmitter and blood vessel relaxant. Recently, it has been reported that low concentration of CO exerts therapeutic actions under various pathological conditions including liver failure, heart failure, gastric cancer, and cardiac arrest. However, little has been known about the effect of CO in neurodegenerative diseases like Parkinson's disease (PD). To test whether CO could exert a beneficial action during oxidative cell death in PD, we examined the effects of CO on 6-hydroxydopamine (6-OHDA)-induced cell death in C6 glioma cells. Treatment of CO-releasing molecule-2 (CORM-2) significantly attenuated 6-OHDA-induced apoptotic cell death in a dose-dependent manner. CORM-2 treatment decreased Bax/Bcl2 ratio and caspase-3 activity, which had been increased by 6-OHDA. CORM-2 increased phosphorylation of NF-E2-related factor 2 (Nrf2) which is a transcription factor regulating antioxidant proteins. Subsequently, CORM-2 also increased the expression of heme oxygenase-1 and superoxide dismutases (CuZnSOD and MnSOD), which were antioxidant enzymes regulated by Nrf2. These results suggest that CO released by CORM-2 treatment may have protective effects against oxidative cell death in PD through the potentiation of cellular adaptive survival responses via activation of Nrf2 and upregulation of heme oxygenase-1, leading to increasing antioxidant defense capacity.

• Korean Journal of Clinical Laboratory Science
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• v.52 no.4
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• pp.408-416
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• 2020

This study examined the neuronal cytotoxicity of aluminum chloride (AlCl3), a dementia inducer, and the protective effects of Aster yomena (Kitam.)(AY) extract on AlCl3-induced cytotoxicity in cultured C6 glioma cells. The antioxidative effects, such as the inhibitory ability of xanthine oxidase (XO) and superoxide anion-radical (SAR) scavenging ability, on cell viability were examined. AlCl3 decreased the cell viability significantly in a dose-dependent manner, and the XTT50 value was 130.0 μM in these cultures. The cytotoxicity of AlCl3 was determined to be mid-toxic according to the Borenfreund and Puerner' toxic criteria. Quercetin (QU), an antioxidant, increased the cell viability reduced by AlCl3-induced cytotoxicity. The protective effect of the AY extract on AlCl3-induced cytotoxicity was analyzed. The AY extract increased the cell viability remarkably compared to the AlCl3-treated group and showed the inhibitory ability of XO and SAR-scavenging ability. The cytotoxicity of AlCl3 was correlated with oxidative stress, and the AY extract effectively prevented AlCl3-induced cytotoxicity through its antioxidative effects. In conclusion, natural resources, such as the AY extract, may be a putative agent for improving the cytotoxicity of heavy metallic compounds correlated with oxidative stress, such as AlCl3, a morbid agent.

• Journal of Pharmacopuncture
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• v.12 no.2
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• pp.31-40
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• 2009

Objective : This study was carried out to investigate protective effects of Pharmacopuncture Solutions (PSs) made by Carthmi Flos (CF), Cnidii Rhizoma (CR) and Astragali Radix (AR) on C6 glioma cells Methods : We investigated the effects of PSs on proliferation rates and types of C6 cells, and also investigated the effects on LDH release. In addition, protective effects of PSs on oxidative stress induced by hydrogen peroxide and SOD-like activities were also investigated. Results : PSs made by CF, CR and AR did not show cytotoxicity in various concentrations. CF-PS and AR-PS elevated levels of proliferation rates significantly. Treatment with CF-PS lowered level of LDH release in C6 cells. In addition, CF-PS and CR-PS showed protective effects on cell death induced by hydrogen peroxide respectively. Finally, CF-PS group showed high level of SOD-like activity compared to that in CR-PS group. Conclusion : These results suggest that CF-PS can accelerate proliferation of neuroglial cells, and has protective action against oxidative stress, which was involved in anti-oxidative effects such as SODlike activities. In addition, CR has protective effects against oxidative stress, and AR can accelerate proliferation of neuroglial cells.

• BMB Reports
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• v.37 no.4
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• pp.480-486
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• 2004

Brain ischemia brings about hypoxic insults. Hypoxia is one of the major pathological factors inducing neuronal injury and central nervous system infection. We studied the involvement of mitogen-activated protein (MAP) kinase in hypoxia-induced apoptosis using cobalt chloride in C6 glioma cells. In vitro cytotoxicity of cobalt chloride was tested by MTT assay. Its $IC_{50}$ value was $400\;{\mu}M$. The DNA fragment became evident after incubation of the cells with $300\;{\mu}M$ cobalt chloride for 24 h. We also evidenced nuclear cleavage with morphological changes of the cells undergoing apoptosis with electron microscopy. Next, we examined the signal pathway of cobalt chloride-induced apoptosis in C6 cells. The activation of extracellular signal-regulated protein kinase 1/2 (ERK 1/2) started to increase at 1 h and was activated further at 6 h after treatment of 400 M cobalt chloride. In addition, pretreatment of PD98059 inhibited cobalt chloride-induced apoptotic cell morphology in Electron Microscopy. These results suggest that cobalt chloride is able to induce the apoptotic activity in C6 glioma cells, and its apoptotic mechanism may be associated with signal transduction via MAP kinase (ERK 1/2).

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.6
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• pp.1190-1196
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• 2002

Selaginella Tamariscina is widely used in the traditional oriental herbal medicine for its anti-inflammatory, anti-cancer effects. The effects of aqueous extracts of Selaginella Tamariscina (ST) on the cell viability and induction of apoptotic cell death were investigated in A549, Raw 264.7, C6-glioma. Jurkat and HL-60 cells. The cell viability after treating with extract of Selaginella Tamariscina was quantified by MTT assay method. The results showed that ST decreased the cell viability in HL-60 and Jurkat cells not in A549, Raw 264.7 and C6-glioma cells. And we also observed the chromatin condensation and DNA fragmentation in HL-60 and Jurkat cells. The enzyme activity of caspase-3, tightly regulated by an apoptosis activating complex, were markedly increased in HL-60 cells treated with the ST by dose-dependent manner. In conclusion, our results suggest that the extract of Selaginella Tamariscina may induce the selective apoptotic cell death in HL-60 and Jurkat cells via activation of caspase-3.

• Herbal Formula Science
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• v.15 no.1
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• pp.213-228
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• 2007

Objectives : The purpose of this report was to investigate the chemotherapeutic effect of Bujeonghangamtang against cancer cells. Materials and Methods : Various cancer cell lines including PANC-1, C6 glioma, SH-SY5Y, HepG2, and MCF-7 cells, were used. Apoptosis was determined by DAPI nuclei staining and flow cytometry in PANC-1 cells treated with 1 mg/ml Bujeonghangamtang for 48 hr. Expression of cell cycle arrest mediators including, cdc2p34 and cyclin B1 proteins were measured by Western blot analysis. Mitochondrial membrane potential was measured by fluorescence staining with JC-1, rhodamine 123. Result : Bujeonghangamtang induced the apoptosis of PANC-1, which was characterized as nucleic acid and genomic DNA fragmentation, chromatin condensation, and sub-G0/G1 fraction of cell cycle increase. but not C6 glioma, SH-SY5Y, HepG2, and MCF-7 cells. PANC-1 cells were markedly sensitive to Bujeonghangamtang. Treatment with Bujeonghangamtang resulted in the decreased expression of cdc2p34 and cyclin B1. Treatment with Bujeonghangamtang also increased the ROS production and induced mitochondrial dysfunction. Conclusion : Bujeonghangamtang exerted cytotoxicity against human Pancreatic cancer cells via cell cycle arrest-mediated apoptotic signaling including ROS production and mitochondrial dysfunction. Our data suggest that Bujeonghangamtang may be an important modulator of chemosensitivity of cancer cells against anticancer chemotherapeutic agents.

• Korean Journal of Clinical Laboratory Science
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• v.54 no.4
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• pp.298-306
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• 2022

This study sought to evaluate the mechanism of cellular injury caused by ferrous sulfate (FeSO₄) and the protective effects of Parnassia palustris L. (PP) extract against FeSO₄-induced cytotoxicity of cultured C6 glioma cells. FeSO₄ is known to cause neurotoxicity and induce Parkinson's disease. The antioxidative effects of PP, such as superoxide dismutase (SOD)-like and superoxide anion-radical (SAR)-scavenging activities, as well as effects on cell viability, were studied. FeSO₄ significantly decreased cell viability in a dose-dependent manner and the XTT₅₀ value, the concentration of FeSO₄ which reduced the cell viability by half, was measured at 63.3 μM in these cultures. FeSO₄ was estimated to be highly cytotoxic by the Borenfreund and Puerner toxicity criteria. Quercetin, an antioxidant, significantly improved cell viability, damaged by FeSO₄-induced cytotoxicity. While evaluating the protective effects of the PP extract on FeSO₄-induced cytotoxicity, it was observed that the extract significantly increased cell viability compared to the FeSO₄-treated group. Also, the PP extract showed superoxide dismutase (SOD)-like and superoxide anion radical (SAR)-scavenging activities. Based on these findings, it can be concluded that FeSO₄ induced oxidative stress-related cytotoxicity, and the PP extract effectively protected against this cytotoxicity via its antioxidative effects. In conclusion, natural antioxidant sources such as PP may be agents useful for preventing oxidative stress-related cytotoxicity induced by heavy metal compounds such as the FeSO₄, a known Parkinsonism inducer.