• Title/Summary/Keyword: neuronal protective effect

검색결과 209건 처리시간 0.031초

Protective effect of Samultang and its four herbal plants against reactive oxygen species in vitro and cellular system

  • Nam, Mi Na;Lee, Ah Young;Sin, Seung Mi;Goo, Young-Min;Cho, Eun Ju
    • 농업과학연구
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    • 제46권3호
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    • pp.427-437
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    • 2019
  • Oxidative stress and overproduction of free radicals have been reported to be a major pathological hallmark of neurodegenerative diseases. Samultang has been known as a beneficial agent to treat liver disease and cardiovascular diseases. However, the anti-oxidant activities and neuro-protective effects of Samultang against oxidative stress still have not been evaluated yet. The aim of the present study was to investigate the anti-oxidant and protective effects of Samultang and its four herbal plants, Paeonia lactiflora (PL), Ligusticum striatum (LS), Rehmannia glutinosa (RG), and Angelica gigas (AG), in vitro system and in SH-SY5Y neuronal cells. The extracts of Samultang strongly increased the radical scavenging activities of 1,1-diphenyl-2-picrylhydrazyl (DPPH), hydroxyl radical (${\cdot}OH$), and nitric oxide (NO) in a concentration-dependent manner. Furthermore, we investigated the protective effects of Samultang on cellular damage against oxidative stress induced by hydrogen peroxide ($H_2O_2$) in SH-SY5Y cells. Treatment with Samultang alleviated the oxidative stress from $H_2O_2$ by increasing the cell viability and decreasing the intracellular reactive oxygen species levels. Based on these results, we further investigated the radical scavenging effects of PL, LS, RG, and AG. In our results, PL had the highest DPPH, ${\cdot}OH$, and NO radical scavenging activities. Thus, PL has a crucial role in Samultang, which has anti-oxidative and neuro-protective effects. The present research suggests that Samultang and PL have protective roles against oxidative stress from $H_2O_2$-induced neuronal cell death.

자색고구마 추출물의 항산화 효과 및 신경세포 보호효과 (Antioxidant and Neuronal Cell Protective Effect of Purple Sweet Potato Extract)

  • 곽지현;최귀남;박주희;김지혜;정희록;정창호;허호진
    • 농업생명과학연구
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    • 제44권2호
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    • pp.57-66
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    • 2010
  • 자색고구마 추출물의 항산화 효과와 산화적 스트레스로 유도된 PC12 신경세포에 대한 보호효과에 대하여 연구하였다. 자색고구마 추출물의 총 페놀함량은 44.25 mg/g, monomeric anthocyanin 함량은 2,394 mg/L로 나타났다. 자색고구마 추출물의 1,1-diphenyl-2-picrylhydrazyl (DPPH), 2,2'-azino-bis-(3-ethylben-zthiazoline-6-sulfonic acid) (ABTS) radical 소거활성, ferric reducing/antioxidant power (FRAP) 및 환원력은 농도 의존적으로 항산화 활성이 증가하였다. MTT {3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyl-tetrazoliumbromide} reduction assay를 이용하여 자색고구마 추출물의 신경세포 보호효과를 측정한 결과, 세포 생존율이 두드러지게 증가하는 것으로 나타났다. 산화적 스트레스는 신경세포막 손상 정도를 증가시키기 때문에 lactate dehydrogenase (LDH) release assay와 neutral red uptake assay를 이용하여 세포막 손상 보호효과를 조사한 결과 자색고구마 추출물 처리구는 대조구에 비하여 산화적 스트레스로 유도된 세포막 손상 보호효과가 농도 의존적으로 나타났다. 따라서 자색고구마 추출물은 천연 항산화 소재 및 알츠하이머성 치매와 같은 신경퇴행성 질환의 예방 소재로서의 활용 가능성이 기대된다.

PC12 손상 세포 및 전뇌허혈 유발 Gerbil에 대한 시호 세포보호효과 (Protective Effect of Bupleuri Radix on Hypoxia Reperfusion Induced by PC12 Cell Damage and Global Ischemia in Gerbil)

  • 최삼열;정승현;신길조;문일수;이원철
    • 대한한의학회지
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    • 제23권4호
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    • pp.113-124
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    • 2002
  • Objects: This research was conducted to investigate the protective effect of Bupleuri Radix against ischemic damage using PC12 cells and global ischemia in gerbils, Methods: To observe the protective effect of Bupleuri Radixon ischemic damage, viability and changes in activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase and production of malondialdehyde (MDA) were observed after treating PC12 cells with Bupleuri Radix during ischemic damage. Gerbils were divided into three groups: a normal group, a 5-minute two-vessel occlusion (2VO) group and a Bupleun Radix administered group after 2VO. The CCAs were occluded by microclip for 5 minutes, Bupleuri Radix was administered orally for 7 days after 2VO. Histological analysis was performed on the 7th day. For histological analysis, the brain tissue was stained with 1 % of cresyl violet solution. Results: 1. Bupleuri Radix has a protective effect against ischemia in the CA1 area of the gerbil's hippocampus 7 days after 5-minute occlusion. 2. In the hypoxia/reperfusion model using PC12 cells, the Bupleuri Radix has a protective effect against ischemia in the dose of 0.2{\;}\mu\textrm{g}/ml,2{\;}\mu\textrm{g}/ml{\;}and{\;} 20{\;}\mu\textrm{g}/ml$. 3. Bupleuri Radix increased the activities of glutathione peroxidase and catalase. 4. The increased activity of superoxidedismutase (SOD) by ischemic damage might have been induced as an act of self-protection. This study suggests that Bupleuri Radix has some neuroprotective effect against neuronal damage following cerebral ischemia in vivo with a widely used experimental model of cerebral ischemia in Mongolian gerbils. Bupleuri Radix also has protective effect on a hypoxia/reperfusion cell culture model using PC12 cells. Conclusions: Bupleuri Radix has protective effect against ischemic brain damage during the early stages of ischemia.

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Pharmacological Properties of CDBT in Hypoxia-induced Neuronal Cell Injury and Their Underlying Mechanisms

  • Park, Sang-kyu;Jung, Eun-sun;Cha, Ji-yoon;Cho, Hyun-kyoung;Yoo, Ho-ryong;Kim, Yoon-sik;Seol, In-chan
    • 대한한방내과학회지
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    • 제40권3호
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    • pp.425-442
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    • 2019
  • Objectives: This study aimed to reveal the pharmacological properties of the newly prescribed herbal mixture, Chenmadansamgamibokhap-tang(CDBT), against hypoxia-induced neuronal cell injury (especially mouse hippocampal neuronal cell line, HT-22 cells) and their corresponding mechanisms. Methods: A cell-based in vitro experiment, in which a hypoxia condition induced neuronal cell death, was performed. Various concentrations of the CDBT were pre-treated to the HT-22 cells for 4 h before 18 h in the hypoxia chamber. The glial cell BV-2 cells were stimulated with $IFN{\gamma}$ and LSP to produce inflammatory cytokines and reactive oxygen species. When the neuronal HT-22 cells were treated with this culture solution, the drug efficacy against neuronal cell death was examined. Results: CDBT showed cytotoxicity in the normal condition of HT-22 cells at a dose of $125{\mu}g/mL$ and showed a protective effect against hypoxia-induced neuronal cell death at a dose of $31.3{\mu}g/mL$. CDBT prevented hypoxia-induced neuronal cell death in a dose-dependent manner in the HT-22 cells by regulating $HIF1{\alpha}$ and cell death signaling. CDBT prevented neuronal cell death signals and DNA fragmentation due to the hypoxia condition. CDBT significantly reduced cellular oxidation, cell death signals, and caspase-3 activities due to microglial cell activations. Moreover, CDBT significantly ameliorated LPS-induced BV-2 cell activation and evoked cellular oxidation through the recovery of redox homeostasis. Conclusions: CDBT cam be considered as a vital therapeutic agent against neuronal cell deaths. Further studies are required to reveal the other functions of CDBT in vivo or in the clinical field.

Kynurenic Acid (KYNA) Attenuates Oxidative Stress and Mitochondrial damage in 6-OHDA-induced Dopaminergic Neuronal Cell Death

  • Lee, Hyun-Jung;Joo, Wan-Seok;Yeo, Joo-Hong;Lee, Kwang-Gill;Chae, Hee-Sun;Kang, Yong-Koo;Lee, In-Sook;Kweon, Hae-Yong;Lee, Ang-Hyung;Kim, Sung-Su
    • 한국잠사학회:학술대회논문집
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    • 한국잠사학회 2003년도 International Symposium of Silkworm/Insect Biotechnology and Annual Meeting of Korea Society of Sericultural Science
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    • pp.112-113
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    • 2003
  • Kynurenic acid (KYNA), tryptophan metabolite is known to have cell protective effect against various insults in the brain. But so far, the protective mechanism is largely unknown. In this study, we investigated how the KYNA exerts protective effect against 6-OHDA, a causative molecule of Parkinsonian syndrome, using SH-SY5Y cells. (omitted)

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키누레닌 대사산물에 의한 신경세포 손상에 대한 Magnolol의 보호효과에 대한 연구 (Magnolol Attenuates Neuronal Cell Death Induced by Kynurenine Metabolite)

  • 이창욱;이현정;김도희;장영미;이상형;정윤화;김대진;정윤희;김경용;김성수;이원복
    • 한국약용작물학회지
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    • 제17권2호
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    • pp.145-150
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    • 2009
  • This study investigated the protective roles and mechanism of magnolol, from the stem bark of Magnolia officinalis against potential neurotoxin 3-hydroxykynurenine (3-HK)-induced neuronal cell death. For the evaluation of protective role of magnolol, we examined cell viability, apoptotic nuclei, change of mitochondrial membrane potential and caspase activity in human neuroblastoma SH-SY5Y cells. It was found that 3-HK induces neuronal cell death in the human neuroblastoma SH-SY5Y cell line. The reduced cell viability produced characteristic features such as cell shrinkages, plasma membrane blebbing, chromatin condensation, and nuclear fragmentation. The cells treated with 3-HK showed an increase in the concentration of reactive oxygen species (ROS) as well as in caspase activity. In addition, both are involved in the 3-HK-induced apoptosis. Magnolol attenuated the cell viability reduction by 3-HK in both a dose- and time-dependent manner. Optical microscopy showed that magnolol inhibited the cell morphological features in the 3-HK-treated cells. Furthermore, the increase in the ROS concentration and the caspase activities by 3-HK were also attenuated by magnolol. These results showed that magnolol has a protective effect on the 3-HK induced cell death by inhibiting ROS production and caspase activity.

PC12 손상 세포 및 전뇌허혈 유발 Gerbil에 대한 지실의 세포보호효과 연구 (Protective Effect of Aurantii Immaturus Fructus on Hypoxia Reperfusion Induced by PC12 Cell Damage and Global Ischemia in Gerbil)

  • 김완식;정승현;신길조;문일수;이원철
    • 대한한의학회지
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    • 제24권1호
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    • pp.29-40
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    • 2003
  • Object : This research was performed to investigate the protective effect of Aurantii Immaturus Fructus against ischemic damage using PC12 cells and global ischemia in gerbils. Methods : To observe the protective effect of Aurantii Immaturus Fructus on ischemia damage, viability and changes in activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase and production of malondialdehyde (MDA) were observed after treating PC12 cells with Aurantii Immaturus Fructus during ischemic insult. Gerbils were divided into three groups : a normal group, a 5-min two-vessel occlusion (2VO) group, and an Aurantii Immaturus Fructus administered after 2VO group. The CCAs were occluded by microclip for 5 minutes. Aurantii Immaturus Fructus was administered orally for 7 days after 2VO. The histological analysis was performed at 7 days after the surgery. For histological analysis, the brain tissue was stained with 1% cresyl violet solution. Results : The results showed that 1. Aurantii Immaturus Fructus had a protective effect against ischemia in the CAI area of the gerbil hippocampus 7 days after 5-minute occlusion, 2. In the hypoxia/reperfusion model using PC12 cells, the Aurantii Immaturus Fructus had a protective effect against ischemia in the dose of $0.2{\;}\mu\textrm{g}/ml,{\;}2{\;}\mu\textrm{g}/ml{\;}and{\;}20{\;}\mu\textrm{g}/ml$ 3. Aurantii Immaturus Fructus increased the activities of glutathione peroxidase and catalase, 4. The activity of superoxide dismutase (SOD) was increased by ischemic damage, which might represent self protection. This study suggests that Aurantii Immaturus Fructus has some neuroprotective effect against neuronal damage following cerebral ischemia in vivo with a widely used experimental model of cerebral ischemia in Mongolian gerbils, and it also has protective effects on a hypoxia/reperfusion cell culture model using PCq2 cells. Conclusions : Aurantii Immaturus Fructus has protective effects against ischemic brain damage at the early stage of ischemia.

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PC12 손상 세포 및 전뇌허혈 유발 Gerbil에 대한 백지의 세포보호효과 (Protective Effect of Angelicae Dahuri Radix on Hypoxia Reperfusion Induced by PC12 Cell Damage and Global Ischemia in Gerbil)

  • 이영효;정승현;신길조;문일수;이원철
    • 대한한의학회지
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    • 제24권1호
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    • pp.110-121
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    • 2003
  • Objective : This research was performed to investigate the protective effect of Angelicae Dahuri Radix against ischemic damage using PC12 cells and global ischemia in gerbils. Methods : To observe the protective effect of Angelicae Dahuri Radix on ischemia damage, viability and changes in activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase and production of malondialdehyde (MDA) were observed after treating PC12 cells with Angelicae Dahuri Radix during ischemic insult. Gerbils were divided into three groups : a normal group, a 5-min two-vessel occlusion (2VO) group, and an Angelicae Dahuri Radix administered after 2VO group. The CCAs were occluded by microclip for 5 minutes. Angelicae Dahuri Radix was administered orally for 7 days after 2VO. The histological analysis was performed at 7 days after surgery. For histological analysis, the brain tissue was stained with 1% cresyl violet solution. Results : 1. Angelicae Dahuri Radix has a protective effect against ischemia in the CA1 area of the gerbil hippocampus 7 days after 5-minute occlusion, 2. In the hypoxia/reperfusion model using PC12 cells, Angelicae Dahuri Radix has a protective effect against ischemia in the dose of $0.2\mu\textrm{g}/ml$, $2\mu\textrm{g}/ml$ and $20\mu\textrm{g}/ml$, 3. Angelicae Dahuri Radix increased the activities of glutathione peroxidase and catalase. 4. The activity of superoxide dismutase (SOD) was increased by ischemic damage, which might represent self protection. This study suggests that Angelicae Dahuri Radix has some neuroprotective effect against neuronal damage following cerebral ischemia in vivo with a widely used experimental model of cerebral ischemia in Mongolian gerbils, and it also has protective effects on a hypoxia/reperfusion cell culture model using PC12 cells. Conclusions : Angelicae Dahuri Radix has protective effects against ischemic brain damage at the early stage of ischemia.

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미성숙 진귤 과피 추출물이 신경세포 사멸에 미치는 영향 (Effect of Immature Citrus sunki Peel Extract on Neuronal Cell Death)

  • 고운철;이선령
    • 한국약용작물학회지
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    • 제23권2호
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    • pp.144-149
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    • 2015
  • The peel of Citrus sunki exhibits multiple biological activities such as anti-oxidant, anti-inflammation and anti-obesity, but little is known about neurodegeneration-related activities. In this study, we investigated the protective effect of ethanolic extract from both immature and mature Citrus sunki peel on neuronal cell death. Treatment of the neuroblastoma cell line SH-SY5Y with $MPP^+$, an inducer of Parkinson disease model, increased cell death in a dose dependent manner. Increased levels of active caspase-3 and cleaved PARP were detected. Treatment with immature Citrus sunki peel extract significantly reduced $MPP^+$-induced neurotoxicity. Cytoprotection with immature Citrus sunki peel extract was associated with a decrease in caspase-3 activation and PARP cleavage. In contrast, mature Citrus sunki peel extract had no significant effects. These data suggest that immature Citrus sunki peel extract may exert anti-apoptotic effect through the inhibition of caspase-3 signaling pathway on $MPP^+$-induced neuronal cell death.