• Title/Summary/Keyword: C6 Glial Cell

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Protective Effect of Dodamtanggami-bang on Endoplasmic Reticulum Stress in C6 Glial Cells (도담탕가미방(導痰湯加味方)이 tunicamycin에 의한 소포체 스트레스성 C6 glial 세포사멸에 미치는 영향)

  • Kim, Bong-Sang;Moon, Byung-Soon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.24 no.6
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    • pp.1004-1011
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    • 2010
  • This study was designed to evaluate the protective effects of Dodamtanggami-bang (DDTG) on tunicamycin induced cell death by ER stress in C6 glial cells. Cell viability was measured by MTT assay and LDH release. Apoptosis was determined by caspase activity and flow cytometry in C6 glial cells. Expression of ER stress mediators including, GRP78 and CHOP proteins were measured by Western blot analysis. Tunicamycin induced the apoptosis of C6 glial cells, which was characterized as nucleic acid and caspase-3 activation, PARP cleavage, and sub-G0/G1 fraction of cell cycle increase. However, pretreatment with DDTG protected C6 glial cells from tunicamycin. Treatment with tunicamycin resulted in the increased the expression of GRP78 and CHOP protein and produced ROS generation. However, pretreatment with DDTG inhibited the ER stress pathway, including increase of the expression of GRP78, CHOP proteins in C6 glial cells treated with tunicamycin. Taken together, these data suggest that DDTG is able to protect C6 glial cells from tunicamycin with marked inhibition of ER stress.

Protective Effect of Palmul-tang on Glutamate Induced Cytotoxicity in C6 Glial cells (Glutamate로 유도된 C6 glial 세포의 독성에 대한 팔물탕(八物湯)의 보호 효과)

  • Shin, Yong-Jeen;Shin, Sun-Ho
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.26 no.4
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    • pp.475-482
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    • 2012
  • This study was designed to elucidate the mechanism of the cytoprotective effect of the Palmul-tang (PMT) on glutamate induced cytotoxicity in rat C6 glial cells. We determined the increase of cell viability by PMT on glutamate-induced death of C6 glial cell. On some experiments, glutamate induced cell death to be an apoptotic phenomena characterized by G1 arrest in cell cycle, chromatin condensation, DNA fragmentation in C6 glial cells. However, pre-treatment of PMT inhibited characteristic apoptotic phenomena. One of the main mediator of glutamate-induced cytotoxicity was known to generation of reactive oxigen species. In this study, PMT attenuated generation of reactive oxigen species by glutamate through down-regulation of NOX1 expression in C6 glial cells. Furthermore, PMT regulated Bcl2 families and caspase proteins, which contribute the cell survival or death. This study suggests that PMT may be candidate for both of therapeutic and protective prescription.

Effects of Gwibitang on Glutamate-induced Apoptosis in C6 Glial Cells (귀비탕이 Glutamate에 의한 C6 Glial Cell의 Apoptosis에 미치는 영향)

  • 강익현;이인;한상혁;문병순
    • The Journal of Korean Medicine
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    • v.22 no.4
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    • pp.45-57
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    • 2001
  • Objectives : The water extract of Gwibitang (GBT) has been traditionally used for treatment of psychologic disease and brain damage in Oriental Medicine, This study was designed to investigate the effect of GBT on the glutamate-induced toxicity of rat C6 glial cells. Methods : The cultured cells were pretreated with GBT and exposed to glutamate, The cell damage was assessed by using MTT assay and Hoechst, IC-l staining, Results : GBT had protective effects in glutamate-induced cytotoxicity, which was revealed as apoptosis characterized by chromatic condensation and the loss of mitochondrial membrane potential in C6 glial cells. However, GBT and glutamate had no effect in the activation of caspase family cysteine proteases including caspase-3, -8 and -9 proteasesin C6 glial ce]]s, GBT significantly recovered the depletion of GSH and inhibited the generation of $H_2O_2$ by glutamate in C6 glial cells. In addition, both GBT and antioxidants such as GSH and NAC protected the glutamate-induced cytotoxicity in C6 glial cells, indicating that GBT possibly has antioxidative effect. Moreover, GBT also inhibited the glutamate-induced degradation of $IkB{\alpha}$ in C6 glial cells, This result suggest that GBT has some inhibitory effects on the transcriptional activation of $NF-_{k}B$. Conclusions : GBT has protective effects in glutamate-induced cytotoxicity via an antioxidative mechanism.

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Protective Effects of Dohongsamul-tang on 2-deoxy-D-glucose Induced Autophagic Cell Death in C6 Glial Cells (도홍사물탕(挑紅四物湯)이 C6 신경교세포의 2-DG에 의한 오토파지성 세포사멸에 미치는 영향)

  • Shin, Hak-Soo;Lee, Seung-Geun;Moon, Byung-Soon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.23 no.3
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    • pp.581-589
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    • 2009
  • The water extract of Dohongsamul-tang(DHSMT) has been traditionally used in treatment of ischemic heart and brain diseases in Oriental Medicine. However, little is known about the mechanism by which DHSMT protects C6 glial cells from glucose deprevation induced damages. Therefore, this study was designed to evaluate the protective effects of DHSMT on 2-deoxy-D-glucose induced autophagy of C6 glial cells. Autophagic phenotype is evaluated by fluorescence microscopy and flow cytometry with specific biological staining dyes, including monodansylcadaverine and acridine orange, as well as Western blot analysis with microtubule-associated protein 1 light chain 3(LC3) and Beclin-1. Treatment with 2-deoxy-D-glucose significantly resulted in a decrease of the viability of C6 glial cells and increase of the extracellular LDH release in a dose and time-dependent manner. However, pretreatment with DHSMT protected C6 glial cells from glucose deprivation with 2-deoxy-D-glucose. The author also observed the fact that autophagy phenotype occurred by 2-deoxy-D-glucose in C6 glial cells. Pretreatment with 3-MA, a pharmacological inhibitior of autophagy, abolished the formation of acidic vesicle organelle in C6 glial cells treated with 2-deoxy-D-glucose. However, pretreatment with DHSMT inhibited the formation of autophagic phenotypes, including formation of acidic vesicle organelle, and increase of the expression of LC-3 II Beclin-1 proteins in C6 glial cells treated with 2-deoxy-D-glucose. Taken together, these data suggest that DHSMT is able to protect C6 glial cells from glucose deprivation with marked inhibition of autophagy formation.

Effect of Yukgunja-tang on Glutamate-induced Apoptosis in C6 Glial Cells (육군자탕(六君子湯)이 Glutamate에 의한 C6 신경교세포의 Apoptosis에 미치는 영향)

  • Jang, Won-Seok;Shin, Yong-Jeen;Ko, Seok-Jae;Ha, Ye-Jin;Kwon, Young-Mi;Shin, Sun-Ho
    • The Journal of Internal Korean Medicine
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    • v.31 no.3
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    • pp.586-599
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    • 2010
  • Objective : The water extract of Yukgunja-tang(YGJT) has been traditionally used in treatment of qi deficiency and phlegm in Oriental medicine. However, little is known about the mechanism by which YGJT protects neuronal cells from injury damages. Therefore, this study was designed to evaluate the protective effects of YGJT on C6 glial cells by glutamate-induced cell death. Methods : The present study describes glutamate, which is known as an excitatory neurotransmitter, related with oxidative damages, and YGJT, which shows protective effects against glutamate-induced C6 glial cell death. One of the main mediators of glutamate-induced cytotoxicity was known on the generation of reactive oxygen species(ROS) via activation of NADPH oxidase (NOX). The protective effects of antioxidant(NAC) and NOX inhibitor(apocynin) on the glutamate-induced C6 glial cells were determined by a MTT reduction assay. Result : YGJT inhibited glutamate-induced ROS generation via inhibition of NOX expression on glutamate-stimulated C6 glial cells. Furthermore, YGJT attenuated glutamate-induced caspase activation. These results suggest that YGJT could be a new potential candidate against glutamate-induced oxidative stress and cell death. Conclusion : These findings indicate that in C6 glial cells, ROS plays an important role of glutamate-induced cell death and that YGJT may prevent cell death from glutamate-induced cell death by inhibiting the ROS generation.

Protective Effects of Ukyium(우귀음, Yougui-yin) in Zinc-induced Apoptosis of C6 Glial Cells (우귀음이 Zinc에 의한 신경교세포의 고사(Apoptosis)에 미치는 영향)

  • 이영구;문병순
    • The Journal of Korean Medicine
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    • v.22 no.3
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    • pp.63-73
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    • 2001
  • Objectives : The objective of the current study is to determine the protective effect of Ukyium(Yougui-yin) on the apoptosis induced by zinc. Methods : Zinc is known to generate reactive oxygen species (ROS), including superoxide anion ($O_2$) and hydrogen peroxide ($H_2O_2$), which eventually contribute to cytotoxicity in a variety of cell types. We investigated the viablity of cells, $H_2O_2$ generation, chromatin condensation and nuclear fragmentation in Hoechst dye staining and $IkB-{\alpha}$ degradation in C6 glial cells of $ZnCl_2$ between pretreatment- and not pretreatment-group with Ukyium. The former methods were researched by Time- and Dose-dependent manners. Results : We demonstrated that pretreatment with Ukyium prevented zinc-induced cell death of C6 glial cells and apoptotic characteristics including chromatin condensation and nuclear fragmentation. Ukyium also prevented $H_2O_2-induced$ cell death. We further confirmed that Ukyium decreased zinc-induced generation of $H_2O_2$ and inhibited degradation of $IkB-{\alpha}$ by zinc in C6 glial ceHs. Conclusions : These data indicated that Ukyium (Yougui-yin) prevents zinc-induced apoptotic death of C6 glial cells via inhibition of ROS generation, such as $H_2O_2$ as well as inhibition of $IkB-{\alpha}$ degradation.

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Protective Effects of Chungsimyeonja-eum on Glutamate-induced Apoptosis in C6 Glial Cells (Glutamate로 유도된 C6 glial 세포 자멸사에 대한 청심연자음(淸心蓮子飮)의 보호효과)

  • Ko, Seok-Jae;Shin, Yong-Jeen;Jang, Won-Seok;Ha, Ye-Jin;Lee, Seon-A;Ahn, Min-Seob;Kwon, Oh-Sang;Shin, Sun-Ho
    • The Journal of Internal Korean Medicine
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    • v.31 no.1
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    • pp.54-65
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    • 2010
  • Objective : The water extract of Chungsimyeonja-eum (CSYJE) has traditionally been used in treatments of heart diseases and brain diseases in Oriental medicine. However, little is known about the mechanism by which CSYJE protects neuronal cells from injury damages. Therefore, in this study we attempted to elucidate the mechanism of the cytoprotective effect of the CSYJE extract on glutamate-induced C6 glial cell death. Methods : Cultured cells were pretreated with CSYJE and exposed to glutamate, cell damage was assessed by using MTT assay and propidium iodide (PI), probe 2',7'-dichlorofluorescein diacetate (DCF-DA) staining. Western blotting was performed using anti-procaspase-3 and anti-PARP, respectively. Result : We determined the elevated cell viability by CSYJE extract on glutamate-induced C6 glial cell death. Glutamate induced DNA fragmentation on C6 glial cells but pre-treatment with CSYJE inhibited DNA fragmentation. One of the main mediators of glutamate-induced cytotoxicity was known to generation of reactive oxygen species (ROS). Pre-treatment with CSYJE inhibited this ROS generation from glutamate-stimulated C6 glial cells. Also, we identified that the ROS-induced DCF-DA green fluorescence was reduced by CSYJE pre-treatment. The critical markers of apoptotic cell death are the cleavages of procaspase-3 protease and PARP proteins, so we checked the expression level and cleavages of procaspase-3 protease and PARP proteins. Glutamate-treated C6 glial cells showed the cleavages of procaspase-3 protease and PARP proteins and followed the reduction of expression of these proteins. Conclusion : These findings indicate that CSYJE may prevent cell death from glutamate-induced C6 glial cell death by inhibiting the ROS generation and procaspase-3 and PARP expression.

Effect of Sopung-tang on Glutamate-Induced Apoptosis in C6 Glial Cells (소풍탕(疎風湯)이 Glutamate에 의한 C6 Glial Cell의 Apoptosis에 미치는 영향)

  • Jeong, Seung-Won;Choi, Chul-Won;Kim, Bong-Sang;Moon, Byung-Soon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.22 no.6
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    • pp.1423-1430
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    • 2008
  • The water extract of Sopung-tang(SPT) has been traditionally used for treatment of psycologic disease and brain damage in oriental medicine. However, little is known about the mechanism by which the water extract of SPT rescues cells from these disease. Therefore, this study was designed to investigate the effect of SPT on the glutamate-induced toxicity of rat C6 glial cells. SPT have protective effects in glutamate-induced toxicity, which was revealed as apoptosis characterized by chromatic condensation and fragmentation and the loss of mitochondrial membrane potential in C6 glial cells. Also, SPT have inhibited the active form of caspase-3 and PARP and significantly protected the apoptotic phenomena by glutamate toxicity in C6 glial cells. However, SPT significantly recovered the depletion of GSH and inhibited the generation of ROS by glutamate in C6 glial cells. In addition, both SPT and antioxidants such as GSH and NAC protected the glutamate-induced cytotoxicity in C6 glial cells, indicating that SPT possibly have antioxidative effect. Specially, SPT were showed transcriptional factor significantly increased the activation of NF-${\kappa}B$ using the analysis of NF-${\kappa}B$ luciferase reporter system in C6 glial cells. These NF-${\kappa}B$ activation protected cells from glutamate-induced toxicity to generate the heme oxygenase-1(HO-1). Taken together, we suggest that SPT have protective effects in glutamate-induced toxicity via a antioxidative mechanism.

Antioxidant effects of Cirsium japonicum var. maackii on oxidative stress in C6 glial cells and mice

  • Min Jeong Kim;Byeong Wook Noh;Qi Qi Pang;Sanghyun Lee;Ji-Hyun Kim;Eun Ju Cho
    • Korean Journal of Agricultural Science
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    • v.49 no.1
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    • pp.137-149
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    • 2022
  • We investigated the effects of Cirsium japonicum var. maackii (CJM) against oxidative stress-induced C6 glial cells and cognitive impairment in mice. To evaluate the anti-oxidative effect of the extract and fractions from CJM, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), reactive oxygen species (ROS), and nitric oxide (NO) assays were conducted in H2O2-treated C6 glial cells. Furthermore, we identified the protective mechanisms of CJM with a scopolamine-treated mice model. The results revealed that H2O2 decreased the cell viability in C6 glial cells, indicating that H2O2 induced oxidative stress in glial cells. However, CJM fractions significantly increased cell viability in H2O2-treated C6 glial cells, which suggested that CJM protected against oxidative stress. CJM extract and fractions also reduced ROS and NO production, which were increased by H2O2 in C6 glial cells. In particular, the EtOAc fraction from CJM (EACJM) effectively protected against oxidative stress by increasing the cell viability and decreasing ROS and NO. Therefore, we carried out further in vivo experiments with EACJM. Scopolamine caused increases of ROS, thiobarbituric acid reactive substances (TBARS), and NO production. However, EACJM effectively alleviated ROS, TBARS, and NO levels compared to scopolamine-injected mice. In addition, EACJM up-regulated protein expressions of superoxide dismutase and glutathione peroxidase, indicating that EACJM enhanced the antioxidative system. Our results demonstrated that CJM had protective effects against oxidative stress in glial cells and memory dysfunction in mice. Based on these results, we propose that CJM could be a potential AD preventive and therapeutic agent.

Effects of Sebsaeng-eum(Shesengyin) on the NO Production of $C_6$ Glial Cell (섭생음이$C_6$ glial 세포의 NO 생성에 미치는 영향)

  • 임창용;김요한;박세홍;이소영;이상관;성강경
    • The Journal of Korean Medicine
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    • v.21 no.4
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    • pp.84-92
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    • 2000
  • Objectives : The water extract of Sebsaeng-eum(SheShengYin) has been used for treatment of ischemic brain damage in oriental medicine, However, little is known about the mechanism by which the water extract of Sebsaeng-eum(SheShengYin) rescues brain cells from ischemic damages. Methods : To elucidate the protective mechanism on ischemic induced cytotoxicity, We investigated the regulation of LPS and PMA induced iNOS expression in $C_{6}$ glial cells. Results : LPS and PMA treatment for 48 h in $C_{6}$ glial cells markedly induced NO, but treatment of the cells with the water extract of Sebsaeng-eum(SheShengYin) decreased nitrite formation. In addition, LPS and PMA treatment for 48 h induced severe cell death in $C_{6}$ glial cells. However treatment of the cells with the water extract of Sebsaeng-eum(SheSheng Yin) did not induce significant changes compared to the control. LPS and PMA induced iNOS activation in $C_{6}$ glial cells caused chromosomal condensation and fragmentation of nuclei. Conclusions : Taken together, We suggest that the protective effects of the water extract of Sebsaeng-eum(SheShengYin) against ischemic brain damages may be mediated by regulation of iNOS during ischemic condition.

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