• Title/Summary/Keyword: Reactive oxigen species

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Microarray Analysis of Gene Expression in Glioblastoma Cells Treated with Gwakhyangjeonggisan Herbal Acupuncture Solution (곽향정기산 약침액이 유해산소로 손상된 Glioblastoma 세포주의 유전자발현에 미치는 영향)

  • Lee, Hong-Seok;Yin, Chang-Shik;Koh, Hyeong-Gyun
    • Journal of Acupuncture Research
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    • v.22 no.6
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    • pp.111-123
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    • 2005
  • Objectives : Neurological disorders have been one of main therapeutic targets of acupuncture. The present study investigated the protective effects of Gwakhyangjeonggisan herbal acupuncture solution (GHAS). Methods : We performed 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay in glioblastoma cells, and did microarray analysis with cells exposed to reactive oxigen species (ROS) of hydrogen peroxide by 8.0 k Human cDNA, with cut-off level of 2-fold changes in gene expression. Results : MTT assay showed protective effect of GHAS on the glioblastoma cells exposed to hydrogen peroxide. When glioblastoma cells were exposed to hydrogen peroxide, 16 genes were upregulated. When the cells were pretreated with GHAS before exposure to hydrogen peroxide, 22 genes were upregulated. Most of the genes upregulated by hydrogen peroxide stimulation were reversed to downregulation by GHAS. Conclusion : The gene expression changes observed in the present study are supposed to be related to the protective molecular mechanism of GHAS in the glioblastoma cells exposed to ROS stress.

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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.

Protective Effects of Ginkgo Biloba Leaf Extract(GBE) against 1,2,4-benzenetriol Induced Toxicity in Vitro (Ginkgo biloga 잎 추출물의 1,2,4-benzenetriol에 대한 항산화 효과에 대한 연구)

  • 이영준;김태연;정해원
    • Journal of Environmental Health Sciences
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    • v.27 no.1
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    • pp.124-130
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    • 2001
  • Ginkgo biliba has been used for bronchitis and asthma in oriental countries and its leaf extract(GBE) contains 24% ginkgoflavone glycoside and 6% terpenoid. Flavonoids and terpenoids are known to have various antioxidant effects such as scavenging of free radicals and chelation of transtional metals. Antioxidant effect of GBE against 1,2,4-benzenetriol(BT), one of toxic metabolites of benzene, was demonstrated throughbsister chromatid exchange(SCE) analysis, single cell gel electrophoresis(SCGE) analysis, DNA cleavage assay and lipid peroxidation production analysis. The means of SCE frequencies at 10, 25 and 50$\mu$M concentration of BT were 7.72, 8.02, 9.22 respectively. In addition of GBE with concentration of 50, 200 and 500$\mu\textrm{g}$/$m\ell$, SCE frequencies were decreased significantly.(p<0.05) According to SCGE analysis, BT induced DNA damage in a dose-dependent manner at concentration of 10 and 50 $\mu$m and the DNA damage induced by BT was significantly protected by GBE(p<0.001). No genotoxicity was observed by GBE treatment alone on DNA cleavage. The effect of BT on lipid peroxidation product, Malondiadehyde(MDA), was increased with concentration of BT(10 and 50 $\mu$M) and reduction in MDA was noted when GBE was added. From above results it is suggested that GBE could protect the cell and DNA from pro-oxidant effect by reactive oxigen species induced by BT.

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Protective Effect of Gwakhyangjeonggisan Herbal Acupuncture Solution in Glioblastoma Cells: Microarray Analysis of Gene Expression (Glioblastoma 세포주의 유해산소 손상을 억제하는 곽향정기산 약침액의 효과에 대한 마이크로어레이 연구)

  • Lee, Hong-Seok;Yin, Chang-Shik;Koh, Hyeong-Gyun
    • Journal of Pharmacopuncture
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    • v.8 no.3
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    • pp.57-69
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    • 2005
  • Objectives : Neurological disorders have been one of main therapeutic targets of acupuncture. The present study investigated the protective effects of Gwakhyangjeonggisan herbal acupuncture solution (GHAS). Methods : We performed 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay in glioblastoma cells, and did microarray analysis with cells exposed to reactive oxigen species (ROS) of hydrogen peroxide by 8.0 k Human cDNA, with cut-off level of 2-fold changes in gene expression. Results : MTT assay showed protective effect of GHAS on the glioblastoma cells exposed to hydrogen peroxide. When glioblastoma cells were exposed to hydrogen peroxide, 24 genes were downregulated. When the cells were pretreated with GHAS before exposure to hydrogen peroxide, 46 genes were downregulated. Many of the genes downregulated by hydrogen peroxide stimulation were decreased in the amount of downregulation or reversed to upregulation. Conclusions : The gene expression changes observed in the present study are supposed to be related to the protective molecular mechanism of GHAS in the glioblastoma cells exposed to ROS stress.

Effect of Kamicheonmagudeungeum on Hypertension (가미천마구등음이 고혈압 병태모델에 미치는 영향)

  • Song, Byoung-Yong;Hong, Suk;Kim, Dong-Hee;Jeon, Sang-Yun
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.21 no.2
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    • pp.504-510
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    • 2007
  • Kamicheonmagudeungeum(KCGE), a traditional herbal medicine, has been used as a therapeutic agent for the treatments of acute stage of hypertension. We evaluated the effects of KCGE on hypertension induced by DOCA-salt in rats. The systolic blood pressure and pulse rate significantly lowered by oral administration with KCGE. The levels of plasma hormones including dopamine, epinephrine and norepinephrine, and serum electrolyte were also reduced in KCGE treated rats. In addition, the production of reactive oxigen species (ROS) were greatly decreased by the treatment with KCGE in cultured bovine endothelial cells and angiotensine converting enzyme (ACE) activites were also inhibited by KCGE in a dose dependent manner. This study indicated that KCGE is a safe and effective treatment for hypertension.

Contribution of HSP90 Cleavage to the Cytotoxic Effect of Suberoylanilide Hydroxamic Acid In Vivo and the Involvement of TXNIP in HSP90 Cleavage

  • Sangkyu Park;Dongbum Kim;Haiyoung Jung;In Pyo Choi;Hyung-Joo Kwon;Younghee Lee
    • Biomolecules & Therapeutics
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    • v.32 no.1
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    • pp.115-122
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    • 2024
  • Heat shock protein (HSP) 90 is expressed in most living organisms, and several client proteins of HSP90 are necessary for cancer cell survival and growth. Previously, we found that HSP90 was cleaved by histone deacetylase (HDAC) inhibitors and proteasome inhibitors, and the cleavage of HSP90 contributes to their cytotoxicity in K562 leukemia cells. In this study, we first established mouse xenograft models with K562 cells expressing the wild-type or cleavage-resistant mutant HSP90β and found that the suppression of tumor growth by the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) was interrupted by the mutation inhibiting the HSP90 cleavage in vivo. Next, we investigated the possible function of thioredoxin interacting protein (TXNIP) in the HSP90 cleavage induced by SAHA. TXNIP is a negative regulator for thioredoxin, an antioxidant protein. SAHA transcriptionally induced the expression of TXNIP in K562 cells. HSP90 cleavage was induced by SAHA also in the thymocytes of normal mice and suppressed by an anti-oxidant and pan-caspase inhibitor. When the thymocytes from the TXNIP knockout mice and their wild-type littermate control mice were treated with SAHA, the HSP90 cleavage was detected in the thymocytes of the littermate controls but suppressed in those of the TXNIP knockout mice suggesting the requirement of TXNIP for HSP90 cleavage. We additionally found that HSP90 cleavage was induced by actinomycin D, β-mercaptoethanol, and p38 MAPK inhibitor PD169316 suggesting its prevalence. Taken together, we suggest that HSP90 cleavage occurs also in vivo and contributes to the anti-cancer activity of various drugs in a TXNIP-dependent manner.