• Title/Summary/Keyword: SK-N-MC

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Neuroprotective effect of Aster yomena ethanolic extract in HT-22 and SK-N-MC cells based on antioxidant activity

  • In Young Kim;Jong Min Kim;Hyo Lim Lee;Min Ji Go;Han Su Lee;Ju Hui Kim;Hyun Ji Eo;Chul-Woo Kim;Ho Jin Heo
    • Food Science and Preservation
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    • v.31 no.1
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    • pp.99-111
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    • 2024
  • The antioxidant potentials of ethanolic extracts derived from Aster yomena (A. yomena) were evaluated by assessing their total phenolic and flavonoid contents and radical scavenging activities. Our findings revealed that the 60% ethanolic extract of A. yomena exhibited the most robust antioxidant properties among all extracts tested. Specifically, the IC50 values for the 2,2'-azino-bis (3-ethyl benzothiazoline-6-sulfonic acid) and 1,1-diphenyl-2-picrylhydrazyl radical scavenging activities of the 60% ethanolic extract from A. yomena were determined to be 1,640.30 ㎍/mL and 2,655.10 ㎍/mL, respectively. Moreover, the inhibitory effect on malondialdehyde increased with the 60% ethanolic extract from A. yomena. To assess the neuroprotective effects, we examined the impact of the 60% ethanolic extract from A. yomena against H2O2-induced cytotoxicity in HT-22 (mouse hippocampal neuronal cell line) and SK-N-MC (human neuroblastoma cell line) cells. The results demonstrated a significant improvement in cell viability and reduced intracellular oxidative stress. Furthermore, the major bioactive compounds present in the 60% ethanolic extract from A. yomena were identified as chlorogenic acid and rutin through high-performance liquid chromatography (HPLC) analysis.

PROTECTION EFFECT OF GINSENG EXTRACT AGAINST APOPTOTIC CELL DEATH INDUCED BY 2,2,5,5-TETRACHLOROBIPHENYL IN NEURONAL SK-N-MC CELLS

  • Lee, Ji-Young;Kim, Jae-Won;Song, Ji-Eun;Kim, Soo-Jung;Chung, Weon-Gu;Kim, Yong-Hoon;Lee, Bo-Ram;Kim, Jin-Hee;Choi, Young-Keun;Joo, Woo-Hong;Cho, Yong-Kweon;Moon, Ja-Young
    • Proceedings of the Korean Society of Toxicology Conference
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    • 2001.10a
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    • pp.112-112
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    • 2001
  • Oxidative stress plays an important role in the pathological process of neurodegenerative diseases. Polychlorinated biphenyls (PCBs) are ubiquitous environmental contaminants, some of which may be neurotoxic. Our previous studies showed that 2,2',5,5'-TetracWorobiphenyl (PCB 52) induced apoptotic death in human neuronal SK-N-MC cells, which was demonstrated on gel electrophoresis by visualization of the proteolytic cleavages of $\beta$-catenin and poly (ADP-ribose) polymerase (PARP) and of the production of characteristic ladder patterns of DNA fragmentation.

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Neuroprotective effects of Momordica charantia extract against hydrogen peroxide-induced cytotoxicity in human neuroblastoma SK-N-MC cells (산화적 스트레스에 대한 여주 (Momordica charantia) 추출물의 항산화 효과 및 세포사멸 억제 기전을 통한 신경세포보호효과)

  • Kim, Kkot Byeol;Lee, Seonah;Heo, Jae Hyeok;Kim, Jung hee
    • Journal of Nutrition and Health
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    • v.50 no.5
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    • pp.415-425
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    • 2017
  • Purpose: Many studies have suggested that neuronal cells protect against oxidative stress-induced apoptotic cell death by polyphenolic compounds. We investigated the neuroprotective effects and the mechanism of action of Momordica charantia ethanol extract (MCE) against $H_2O_2-induced$ cell death of human neuroblastoma SK-N-MC cells. Methods: The antioxidant activity of MCE was measured by the quantity of total phenolic acid compounds (TPC), quantity of total flavonoid compounds (TFC), and 2,2-Diphenyl-1-pycrylhydrazyl (DPPH) radical scavenging activity. Cytotoxicity and cell viability were determined by CCK-8 assay. The formation of reactive oxygen species (ROS) was measured using 2,7-dichlorofluorescein diacetate (DCF-DA) assay. Antioxidant enzyme (SOD-1,2 and GPx-1) expression was determined by real-time PCR. Mitogen-activated protein kinases (MAPK) pathway and apoptosis signal expression was measured by Western blotting. Results: The TPC and TFC quantities of MCE were 28.51 mg gallic acid equivalents/extract g and 3.95 mg catechin equivalents/extract g, respectively. The $IC_{50}$ value for DPPH radical scavenging activity was $506.95{\mu}g/ml$ for MCE. Pre-treatment with MCE showed protective effects against $H_2O_2-induced$ cell death and inhibited ROS generation by oxidative stress. SOD-1,2 and GPx-1 mRNA expression was recovered by pre-treatment with MCE compared with the presence of $H_2O_2$. Pre-treatment with MCE inhibited phosphorylation of p38 and the JNK pathway and down-regulated cleaved caspase-3 and cleaved PARP by $H_2O_2$. Conclusion: The neuroprotective effects of MCE in terms of recovery of antioxidant enzyme gene expression, down-regulation of MAPK pathways, and inhibition apoptosis is associated with reduced oxidative stress in SK-N-MC cells.

Neuroprotective effects of phenolic compounds isolated from Spiraea prunifolia var. simpliciflora (조팝나무(Spiraea prunifolia var. simpliciflora)로부터 분리한 페놀 화합물의 신경세포 보호효과)

  • Oh, Seon Min;Choi, Doo Jin;Kim, Hyoung-Geun;Lee, Jae Won;Lee, Young-Seob;Lee, Jeong-Hoon;Lee, Seung-Eun;Kim, Geum-Soog;Baek, Nam-In;Lee, Dae Young
    • Journal of Applied Biological Chemistry
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    • v.61 no.4
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    • pp.397-403
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    • 2018
  • The leaves of Spiraea prunifolia were extracted with 80% aqueous MeOH and the concentrates were partitioned into EtOAc, n-BuOH, and $H_2O$ fractions. The repeated $SiO_2$ or ODS column, and medium pressure liquid chromatographies for the n-BuOH fraction led to isolation of two phenolic glucosides. The chemical structures of these compounds were determined as isosalicin (1) and crenatin (2) based on spectroscopic analyses including Nuclear magnetic resonance and MS. Extracts were analyzed using UPLC-MS/MS providing a short analysis time within 5 min using MRM technique. The concentration of crenatin was higher as 9.53 mg/g and isosalicin was lower as 0.65 mg/g. Neuroprotective effects of these compounds against hydrogen peroxide ($H_2O_2$)-induced neurotoxicity were evaluated. The results showed that exposure to $H_2O_2$ induced morphological changes, cell death and neurotoxicity in SK-N-MC cells. However, pretreatment with crenatin resulted in inhibition of morphological change, reduction of loss of cell viability and attenuation of neuronal damage. These results suggested that neuroprotective effect of crenatin isolated from S. prunifolia can be a good candidate for the development of health beneficial foods which can ameliorate the degenerative neuronal disease caused by oxidative stress.

Influence of Kamijihwang-hwan on the Hypoxic Damage of Cultured Cerebral Neurons from mouse and SK-N-MC cells (가미지황환이 저산소성 신경세포 손상에 미치는 영향)

  • Kyung Baek Yeun;Ju Sung Min;Kim Kun Jun;Kim Dae Keun;Kang Jeong Ho;Lee Young Chan;Lee Jun;Kim Young Mok;Jeon Byung Hun
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.17 no.4
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    • pp.1082-1091
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    • 2003
  • To elucidate the neuroprotective effect of Kamijihwang-hwan(KSH) on nerve cells damaged by hypoxia, the cytotoxic effects of exposure to hypoxia were determined by XTT, NR, MTT and SRB asssay. The activity of catalase and SOD was measured by spectrophometry, and TNF-α and PKC activity was measured after exposure to hypoxia and treatment of Kamijihwang-hwan(KSH) water extract(KJHWE). Also the neuroprotective effect of KJHWE was researched for the elucidation of neuroprotective mechanism. The results were as follows ; Hypoxia decreased cell viability measured by XTT, NR assay when cultured cerebral neurons were exposed to 95% N2/5% CO₂ for 2~26 minutes in these cultures and KJHWE inhibited the decrease of cell viability. H₂O₂ treatment decreased cell viability measured by MTT, and SRB assay when cultured cerebral neurons were exposed to 1-80 uM for 6 hours, but KJHWE inhibited the decrease of cell viability. Hypoxia decreased catalase and SOD activity, and also TNF-α and PKC activity in these cultured cerebral neurons, but KJHWE inhibited the decrease of the catalase and SOD activity in these cultures. Hypoxia triggered the apoptosis via caspase activation and internucleosomal DNA fragmentation. Also hypoxia stimulate the release of cytochrome c form mitochondria. KJHWE inhibited the apoptosis via caspase activation induced by hypoxia. From these results, it can be suggested that brain ischemia model induced hypoxia showed neurotoxity on cultured mouse cerebral neurons, and the KJHWE has the neuroprotective effect in blocking the neurotoxity induced by hypoxia in cultured mouse cerebral neurons.

Polyethylene flow prediction with a differential multi-mode Pom-Pom model

  • Rutgers, R.P.G.;Clemeur, N.;Debbaut, B.
    • Korea-Australia Rheology Journal
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    • v.14 no.1
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    • pp.25-32
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    • 2002
  • We report the first steps of a collaborative project between the University of Queensland, Polyflow, Michelin, SK Chemicals, and RMIT University, on simulation, validation and application of a recently introduced constitutive model designed to describe branched polymers. Whereas much progress has been made on predicting the complex flow behaviour of many - in particular linear - polymers, it sometimes appears difficult to predict simultaneously shear thinning and extensional strain hardening behaviour using traditional constitutive models. Recently a new viscoelastic model based on molecular topology, was proposed by McLeish and carson (1998). We explore the predictive power of a differential multi-mode version of the porn-pom model for the flow behaviour of two commercial polymer melts: a (long-chain branched) low-density polyethylene (LDPE) and a (linear) high-density polyethylene (HDPE). The model responses are compared to elongational recovery experiments published by Langouche and Debbaut (19c99), and start-up of simple shear flow, stress relaxation after simple and reverse step strain experiments carried out in our laboratory.

Inhibitory Effects of Chungpesagan-Tang on Ischemia/Reperfusion-Induced Inflammatory Responses In vitro (허혈/재관류 환경하에서 청폐사간탕의 염증 관련 반응 억제 효과)

  • Hong, Seong-Gil;Kang, Bong-Joo;Cho, Dong-Wuk
    • Korean Journal of Oriental Medicine
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    • v.6 no.1
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    • pp.81-87
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    • 2000
  • Chungpesagan-Tang (CST), a Korean traditional prescription composed of oriental medical herbs, has been used successfully to improve human health and regimen. This study was designed to examine the inhibitory effects of CST against in vitro ischemia/reperfusion-induced inflammatory response. We have characterized the production of prostaglandin $E_2$ and arachidonic acid during ischemia/reperfusion in the human neuroblastoma SK-N-MC and human monocytic macrophage U937 cells and the inhibitory effect of CST on these inflammation-related substance formation has been found out in this study. This result suggested that CST used in this experiment reinforced antiinflammatory potentials and protected cells against ischemia/reperfusion-induced inflammatory resopnse.

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