• Title/Summary/Keyword: 신경세포보호

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Protective Effect of MeOH Extract of Evodia officinalis on Cyanide-induced Neurotoxicity in Cultured Neuroblastoma Cells (오수유 MeOH 추출물이 Cyanide에 의한 신경세포의 보호효과에 미치는 영향)

  • Kim, Sang-Tae;Ahn, Soung-Hee;Kim, Jeong-Do;Kim, Young-Kyoon
    • Korean Journal of Pharmacognosy
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    • v.34 no.4 s.135
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    • pp.282-287
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    • 2003
  • We reported that neurotoxicity may contribute to cyanide-induced neuronal injury. Cyanide stimulates the release of glutamate which can activate glutamate receptors to propagate excitotoxic processes. We examined the role of plant extracts in mediating the cyanide-induced cytotoxicity and report here that the cytotoxicity assessed in SK- N-SH cell cultures by measuring lactate dehydrogenase (LDH) in the culture media was significantly blocked by Evodia officinalis MeOH extract (OMU). Also, when OMU was treated in NaCN level cultures, the neurite outgrowth was regenerated as much as in the treatment of NaCN only. These results indicate that OMU treatment were not only protected the neurons against NaCN-induced damage but also regenerated the neurite outgrowth of neuroblastoma cells.

The Neuroprotective Effect of Acupuncture Treatment at Shaofu (HT8) on Kainic Acid-induced Epilepsy Mouse Model. (Kainic acid 유발 간질 생쥐모델에서 소부혈(少府穴) 침치료의 해마 신경세포 보호효과연구)

  • Kim, Yoon-Young;Min, Sang-Yeon;Kim, Ji-Yong;Kim, Jang-Hyun
    • The Journal of Korean Medicine
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    • v.31 no.5
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    • pp.167-178
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    • 2010
  • Objectives: The present study investigated the effects of acupuncture treatment and their mechanism by using the kainic acid (KA)-induced epilepsy mouse model. Materials and Methods: The seizure was induced by an intraperitoneal (i.p.) injection of 30 mg/kg KA, and the acupuncture treatment was subsequently administered to acupoint Shaofu(HT8) bilaterally with two pretreatment sessions before injection (total 3 times over 3 days). Twenty four hours after injection, we observed the survival of neuronal cells in the CA3 region of the hippocampus. In addition, the activation of microglia and astrocytes was observed by using CD11b and GFAP immunohistochemistry in the same region. Results: The results indicate that acupuncture treatment reduced the rate of neural cell death in the CA3 region of the hippocampus and decreased the activations of microglia and astrocytes in this region. Conclusion: These results demonstrate that acupuncture treatment protects hippocampal neuronal cell death from KA-induced epileptic seizure by inhibiting the activations of microglia and astrocytes.

Neuroprotective Effect according to Reactive Oxygen Species Scavenging Activity from Extracts of Cudrania tricuspidata Leaves (활성산소 소거활성에 따른 꾸지뽕잎 추출물의 신경세포 보호 효과)

  • Kang, Young-Kyoung;Lee, Eun-Ah;Park, Hae-Ryong
    • Korean journal of food and cookery science
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    • v.28 no.6
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    • pp.821-828
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    • 2012
  • In an attempt to identify the neuroprotective effect of Cudrania tricuspidata (CT) leaves against ROS (reactive oxygen species)-induced oxidative stress in neuronal cells, the extracts from CT leaves were investigated using PC12 cells and N18-RE-105 cells. The methanolic and ethanolic extracts from CT were denoted as CTM (Cudrania tricuspidata Leaves methanolic extracts) and CTE (Cudrania tricuspidata Leaves ethanolic extracts), respectively. The neuroprotective effects of the extracts were measured by DCF-DA assay, MTT reduction assay, and LDH release assay. The PC12 cells exposed to $H_2O_2$-induced oxidative stress and the N18-RE-105 cells exposed to glutamate-induced oxidative stress were treated with various concentrations of CTM and CTE. The results, CTM treatments resulted in the induction of a dose-dependent protective effect in PC12 cells and N18-RE-105 cells. Interestingly, CTE also showed neuroprotective effect in PC12 cells and N18-RE-105 cells. Therefore, these results suggest that CTM and CTE could be a new potential candidate as neuroprotective agents against ROS-induced oxidative stress in neuronal cells.

Antioxidant and Neuronal Cell Protective Effects of Eugenia caryophyllata Thunb. by Extraction Solvent (용매별 정향 추출물의 항산화 및 신경세포 보호 효과)

  • Oh, Hee-Kyung
    • Journal of the Korean Society of Food Culture
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    • v.32 no.6
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    • pp.583-588
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    • 2017
  • This study examined the antioxidant and neuronal cell protective effects of the water and methanol extracts of Eugenia caryophyllata Thunb. The total polyphenol content was significantly higher in the methanol extract than in the water extract. The DPPH radical scavenging activity in the water extract was similar to Vit. C at a concentration of $100{\sim}200{\mu}g/mL$. The ABTS radical scavenging activity in the water and methanol extract was similar to Vit. C at a concentration of $800{\sim}1,000{\mu}g/mL$. The superoxide dismutase (SOD)-like activity in the methanol extract was similar to Vit. C at a concentration of $800{\sim}1,000{\mu}g/mL$. The DPPH, ABTS radical scavenging and (SOD)-like activity increased with increasing extract concentration. In a cell viability using MTT, the water extract (50 and 100 ppm) and methanol extract (100 ppm) had a protective effect against $H_2O_2$-induced neurotoxicity.The result ssuggest that the extract of E. caryophyllata Thunb. has antioxidant activities and may be useful for treating neurodegenerative disorders.

Neuroprotective Activity of Spirulina maxima Hot Ethanol Extract (스피루리나 에탄올 추출물의 신경세포 보호활성)

  • Ryu, Gahee;Ma, Choong Je
    • Korean Journal of Pharmacognosy
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    • v.52 no.3
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    • pp.149-156
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    • 2021
  • Excessive glutamate can cause oxidative stress in neuronal cells and this can be the reason for neurodegenerative disease. In this study, we investigated the protective effect of Spirulina maxima hot ethanol extract on mouse hippocampal HT22 cell of which glutamate receptor has no function. HT22 cells were pre-treated with S. maxima sample at a dose dependent manner (1, 10 and 100 ㎍/ml). After an hour, glutamate was treated. Cell viability, reactive oxygen species (ROS) accumulation, Ca2+ influx, decrease of mitochondrial membrane potential level and glutathione related assays were followed by then. S. maxima ethanol extract improved the cell viability by suppressing the ROS and Ca2+ formation, retaining the mitochondrial membrane potential level and protecting the activity of the antioxidant enzymes compared with group of vehicle-treated controls. These suggest that S. maxima may decelerate the neurodegeneration by attenuating neuronal damage and oxidative stress.

Effect of Gagamjeongji-hwan and Evodiae Fructus on Memory Impairment and Neuronal Damage Induced by Focal Ischemia in the Rat (국소 전뇌 허혈 모델 백서에서 가감정지환(加減定志丸)과 오수유(吳茱萸)가 기억증진과 신경세포보호에 미치는 효과)

  • Kim, Hoi-Young;Son, Hyun-Soo;Kang, Ji-Hong;Choi, U-Jeong;Lee, Jin-Seok;Yang, Jae-Hoon;Seol, Jae-Kyun;Lee, Eon-Jeong
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.22 no.6
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    • pp.1487-1494
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    • 2008
  • This study was conducted to determine the effect of Gagamjeongji-hwan (JJH)(Jiajiandingzhi-wan) and Evoidae Fructus (EF) on learning and memory disturbance and neuronal damage induced by focal ischemia in the rat. Rats were used for testing in the following three. Morris Water Maze, Cholineacetyltransferase (ChAT) immunohistochemistry, acetylcholine esterase (AchE) histochemistry. JJH+ISCH group (ischemia-induced rats pretreated with JJH) and EF+ISCH group (ischemia-induced rats pretreated with EF) significantly reduced the latency of swimming time, compared with those of ISCH group (ischemia-induced rats) in morris water maze acquisition test. JJH+ISCH group attenuated ischemia.induced learning and memory damage in morris water maze retention test. The density of ChAT neurons of the JJH+ISCH and EF+ISCH group in the hippocampal CA1 area was increased, compared to that of SAL+ISCH group (ischemia-induced rats pretreated with SAL). The density of AchE neurons of the JJH+ISCH and EF+ISCH group in the hippocampal CA1 and CA3 area was increased, compared to that of SAL+ISCH group. These results suggest that Gagamjeongji-hwan (JJH) and Evodiae Fructus (EF) may have significant protective effects on ischemia-induced brain damage and memory impairments.

Effect of the neuroprotetion and anti-Alzheimer's disease in CT99-induced Neuro 2A cells by Ikgiansintang water extract (CT99 발현 신경 세포주에서 익기안신탕(益氣安神湯)의 신경보호 및 항치매 효과)

  • Hwang, Yeon-Kyu;Lee, So-Yeon;Yoon, Hyeon-Deok;Shin, Oh-Chul;Park, Chang-Gook;Park, Chi-Sang
    • Herbal Formula Science
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    • v.13 no.1
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    • pp.103-121
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    • 2005
  • Alzheimer's disease(AD) is a geriatric dementia that is widespread in old age. In the near future AD will be the biggest problem in public health service. It has been widely believed that $A{\beta}$ peptide devided from APP causes apoptotic neurotoxicity in AD brain. However, recent evidence suggests that n99 may be an important factor causing neurotoxicity in AD. Mouse Neuro 2A cells expressed with CT99 exhibited remarkable apoptotic cell damage. We invesgated the protective effects of Ikgiansintang water extract(IGA). Findings from our experiment have shown that IGA inhibits the activities of CT99, which has neurotoxicities and apoptotic activities in cell line. In addition treatment of IGA($50{\mu}g/ml$ for 24 hours) partially prevented CT99-induced cytotoxicity in Neuro 2A cells. As the result of this study, In IGA group, the apoptosis in the nervous system is inhibited, the repair against the degerneration of Neuro 2A cells by n99 expression is promoted. Base on these findings, IGA may be beneficial for the treatment of AD.

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Neuroprotective effects of Angelicae Acutilobae Radix water extract against ischemia·reperfusion-induced apoptosis in SK-N-SH neuronal cells (허혈·재관류 유도 신경세포사멸에 대한 일당귀 물추출물의 신경보호효과 연구)

  • Oh, Tae-Woo;Park, Ki-Ho;Lee, Mi-Young;Choi, Go-Ya;Park, Yong-Ki
    • The Korea Journal of Herbology
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    • v.26 no.4
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    • pp.67-74
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    • 2011
  • Objectives : The purpose of the study is to determine the neuroprotective effects of the water extract of Angelicae Acutilobae Radix(AA) on ischemia reperfusion-induced apoptosis in SK-N-SH human brain neuronal cells. Methods: SK-N-SH cells were treated with different concentrations of AA water extract (0.1, 0.2, 0.5 and 1.0 mg/ml) for 2 hr and then stimulated with Dulbecco's phosphate-buffered saline containing CI-DPBS: 3mM sodium azide and 10 mM 2-deoxy-D-glucose for 45 min, reperfused with growth medium, and incubated for 24 h. Cell viability was determined by WST-1 assay, and ATP/ADP levels were measured by ADP/ATP ratio assay kit. The levels of caspase-3 protein were determined by Western blot and apoptotic body was observed by Hoechst 33258 staining. Results : AA extract significantly inhibited decreasing the cell viability in ischemia-induced SK-N-SH cells. AA also increased the ratio of ADP/ATP in ischemia-induced neuronal cells and decreased the expression levels of apoptotic protein, caspase-3 and apoptotic DNA damage. Conclusions : Our results suggest that AA extract has a neuroprotective property via suppressing the apoptosis and increasing the energy levels in neuronal cells, suggesting that AA extract may has a therapeutic potential in the treatment of ischemic brain injury.

Neuroprotective effects of some herbal medicine plant extract against ischemia·reperfusion-induced cell death in SK-N-SH neuronal cells (허혈·재관류 유도성 신경세포사멸에 대하여 신경보호효과를 가지는 약용식물 추출물의 검색)

  • Oh, Tae-Woo;Lee, Mi Young;Lee, Hye Won;Park, Yong-Ki
    • The Korea Journal of Herbology
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    • v.28 no.2
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    • pp.45-53
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    • 2013
  • Objectives : The purpose of the study is to determine the neuroprotective effects of the water and 80% EtOH extract of some herbal medicine plant on ischemia reperfusion-induced cell death in SK-N-SH human brain neuronal cells. Methods : SK-N-SH cells were treated with 3mM sodium azide and 10 mM 2-deoxy-D-glucose for 45 min, ptior to the addition of different concentrations of herbal medicine plant extract (0, 10, 25, 50, 100, 250, 500, 1000 ${\mu}g/ml$) for 2 hr and then reperfused with growth medium, incubated for 24 h. Cell viability was determined by WST-1 assay, and ATP/ADP levels were measured by ADP/ATP ratio assay kit. Results : Herbal medicine plant extract significantly inhibited decreasing the cell viability in ischemia-induced SK-N-SH cells. Also increased the ratio of ADP/ATP in ischemia-induced neuronal cells. Conclusions : Our results suggest that herbal medicine plant extract has a neuroprotective property via increasing the energy levels in neuronal cells, suggesting that extract may has a therapeutic potential in the treatment of ischemic brain injury. The exact component and mechanism remains for the future study.

Neuroprotective Effects of Stachys sieboldii Miq. Extract Against Ischemia/reperfusion-induced Apoptosis in SH-SY5Y Neuroblastoma Cells (허혈-재관류 유도 신경세포사멸에 대한 초석잠 추출물의 신경보호 효과 연구)

  • Young-Kyung Lee;Chul Hwan Kim;Su Young Shin;Buyng Su Hwang;Min-Jeong Seo;Hye Jin Hwang;Kyung-Min Choi;Jin-Woo Jeong
    • Proceedings of the Plant Resources Society of Korea Conference
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    • 2020.08a
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    • pp.76-76
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    • 2020
  • Stachys sieboldii Miq. (chinese artichoke), which has been extensively used in oriental traditional medicine to treat of ischemic stroke; however, the role of Stachys sieboldii Miq. (SSM) in cerebral ischemia/reperfusion (I/R) injury is not yet fully understood. In the current study, the neuroblastoma cell line (SH-SY5Y) were subjected to oxygen-glucose deprivation/reperfusion (OGD/R) to simulate I/R injury in vitro model. The results showed that SSM improved OGD/R-induced inhibitory effect on cell viability of SH-SY5Y Cells. SSM displayed anti-oxidative activity as proved by the decreased levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and increased activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in OGD/R-induced SH-SY5Y Cells. In addition, cell apoptosis was markedly decreased after SSM treatment in OGD/R-induced SH-SY5Y Cells. The up-regulation of Bcl-2 and down-regulation of Bax, thus reducing the Bax/Bcl-2 ratio that in turn protected the activation of caspase-9 and -3, and inhibition of poly (ADP-ribose) polymerase cleavage, which was associated with the blocking of cytochrome c release to the cytoplasm. Collectively, SSM protected human neuroblastoma SH-SY5Y cells from OGD/R-induced injury via preventing mitochondrial-dependent pathway through scavenging excessive ROS, suggesting that SSM might be a potential agent for the ischemic stroke therapy.

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