• Title/Summary/Keyword: neuroprotective effects

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Neuroprotective effects of baicalein. baicalin. and wogonin in primary cultured rat cortical cells

  • Cho, Jung-Sook;DokGo, Hyang;Lee, Kwang-Heun;Lee, Hyung-Kyu
    • Proceedings of the PSK Conference
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    • 2002.10a
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    • pp.302.2-303
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    • 2002
  • Oxidative stress has been implicated in the pathophysiology of many neurodegenerative disorders including Alzheimer's and Parkinson's diseases. Baicalein. baicalin and wogonin. the major constituents of Scutellaria baicalensis. have been reported to exhibit antioxidant properties in many different bioassay systems. The present study evaluated neuroprotective effects of these flavonoids on various neuronal injuries induced in primary cultured rat cortical cells by oxidative stress. NMDA. oxygen-glucose deprivation. and $A{\beta}$(25-35). (omitted)

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Dose-Independent Pharmacokinetics of a New Neuroprotective Agent for Ischemia-Reperfusion Damage, KR-31543, after Intravenous and Oral Administration to Rats: Hepatic and Intestinal First-Pass Effects

  • Lee, Mi-Hye;Lee, Dae-Young;Bae, Soo-Kyung;Kim, Eun-Jung;Kim, Yoon-Gyoon;Kim, Sun-Ok;Lee, Dong-Ha;Lim, Hong;Yoo, Sung-Eun
    • Proceedings of the PSK Conference
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    • 2003.04a
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    • pp.312.2-313
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    • 2003
  • The purpose of this study was to report dose-independent pharmacokinetics of KR-31543, a new neuroprotective agent for ischemia-reperfusion damage, after intravenous and oral administration and first-pass effects after intravenous. intraportal, intragastric, and intraduodenal administration in rats. After intravenous (10, 20 and 50 mg/kg) and oral (10, 20 and 50 mg/kg) administration, the pharmacokinetic parameters of KR-31543 were dose-independent. (omitted)

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Alterations in Motor Activity Induced by High Dose Oral Administration of Dextromethorphan Throughout two Consecutive Generations in Mice

  • Kim, Hyoung-Chun;Jhoo, Wang-Kee
    • Archives of Pharmacal Research
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    • v.18 no.3
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    • pp.146-152
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    • 1995
  • To achieve a better understanding of the effects on behavioral safety caused by possible neuroprotective doses (50 mg/kg, p.o.) of dextromethorphan HBr (DM), several motor activity measures were monitored in two generations of mice through a long-term period of ten months. Adult male mice (G1), in the presence of DM, developed behavioral tolerance after an initial suppression period. Prenatally exposed, second generation (G2) mice formed two groups, prenatal exposure alone (G2C) and prenatally exposed with additional postnatal exposure (G2T). In the presence of DM, group G2T was characterized by significant behavioral impairment; while G2C exhibited behavioral activation. These results suggest that more attention should be given to the prenatal effects of DM on a developing organism.

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Neuroprotective Effects of Bee Venom, which Removes High Molecular Elements against $MPP^+$-induced Human Neuroblastoma SH-SY5Y Cell Death ($MPP^+$로 유도된 SH-SY5Y신경세포 사멸에 대한 고분자성분제거 봉독약침액의 신경보호 효과 연구)

  • Bae, Kwang-Rok;Doo, Ah-Reum;Kim, Seung-Nam;Park, Ji-Yeon;Park, Hi-Joon;Lee, Hye-Jung;Kwon, Ki-Rok
    • The Journal of Internal Korean Medicine
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    • v.31 no.2
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    • pp.254-263
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    • 2010
  • Objectives : The neuroprotective effects of bee venom (BV) have been demonstrated in many studies, but bee venom has many side effects. So we used sweet bee venom (SBV), which has high molecular elements removed to reduce the side effects. I examined the neuroprotective effect of sweet bee venom in 1-methyl-4-phenylpyridine ($MPP^+$)-induced human neuroblastoma SH-SY5Y cells. Methods : To observe the possible toxicity of SBV itself, SH-SY5Y cells were treated with SBV in various concentrations for 3 h and $MPP^+$ in concentrations (1 and 5mM) for 24h. To investigate the protective effect of SBV against $MPP^+$ toxicity, SH-SY5Y cells were pretreated with vehicle or nontoxic concentrations of SBV for 3h and the cells were not washed, followed by incubation with respective concentrations of SBV and 1 mM $MPP^+$ for 24h. To investigate the protective effect of SBV against $MPP^+$ toxicity, SH-SY5Y cells were pretreated with vehicle or nontoxic concentrations of SBV for 3h and the cells were not washed, followed by incubation with respective of SBV(0.5%), 1 mM $MPP^+$, 5uM AKT inhibitor(LY984002) and 10uM ERK inhibitor(PD98059) for 24 h. The protective effect was measured by cell viability assay. To investigate the degree of apoptosis, caspase-3 enzyme activity was measured in control, $MPP^+$, SBV+$MPP^+$. Results : SBV (0.5%) pretreatment protected the SH-SY5Y cells against $MPP^+$-induced apoptotic cell death. The cell viability was higher in the SH-SY5Y cells that were pretreated with vehicle or nontoxic concentrations of SBV than those not pretreated. The caspase-3 activity was lower in the pretreated groups than these not pretreated. ERK and AKT enzymes have a role in the neuroprotective effects of the sweet bee venom. Conclusions : The results demonstrate that SBV has a protective effect on dopaminergic neurons against $MPP^+$ toxicity. This data suggest that SBV could be a potential therapeutic tool for neurodegenerative diseases such as Parkinson's disease(PD).

Anti-Oxidative and Neuroprotective Effects of Rhei Rhizoma on BV-2 Microglia Cells and Hippocampal Neurons (대황(大黃)의 항산화와 신경세포손상 보호효능에 대한 연구)

  • Myung, Sung-Ha;Kim, Youn-Sub
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.19 no.3
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    • pp.647-655
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    • 2005
  • This study demonstrated anti-oxidative and neuroprotective effects of Rhei Rhizoma. Anti-oxidative effects were studied on BV-2 microglia cells damaged by $H_2O_2$ and nitric oxide. Neuroprotective effects were studied by using oxygen/glucose deprivation of the organotypic hippocampal slice cultures. The results obtained are as follows; The groups treated with 0.5 and 5 mg/ml of Puerariae Radix revealed significant decreases of neuronal cell death area and cell death area percentages in CA1 region of ischemic damaged hippocampus cultures during whole 48 hours of the experiment. The group treated with 50 mg/ml of Puerariae Radix demonstrated decreases of neuronal cell death area and cell death area percentages in CA1 region, but these were not significant statistically. The groups treated with 0.5 and 5 mg/ml of Puerariae Radix revealed significant decreases of neuronal cell death area and cell death area percentages in dentate gyrus of ischemic damaged hippocampus cultures during whole 48 hours of the experiment. The group treated with 50 mg/ml of Puerariae Radix demonstrated decreases of neuronal cell death area and cell death area percentages in dentate gyrus, but these were not significant statistically. The groups treated with 0.5 and 5 mg/ml of Puerariae Radix revealed significant decreases of TUNEL-positive cells in both CA1 region and dentate gyrus of ischemic damaged hippocampus cultures. The group treated with 50 mg/ml of Puerariae Radix demonstrated significant decrease of TUNEL-positive cells in CA1 region, but not in dentate gyrus of ischemic damaged hippocampus. The groups treated with 0.5 and 5 mg/ml of Puerariae Radix revealed significant decreases of LDH concentrations in culture media of ischemic damaged hippocampus cultures. The group treated with 50 mg/ml of Puerariae Radix demonstrated decrease of LDH concentrations in culture media, but it was not significant statistically. The groups treated with 0.5 and 5 mg/ml of Puerariae Radix revealed significant increases of cell viabilities of BV-2 microglia cells damaged by $H_2O_2$. The group treated with 50 mg/ml of Puerariae Radix demonstrated increase of cell viability of BV-2 microglia cells, but it was not significant statistically. The group treated with 0.5 mg/ml of Puerariae Radix revealed significant increase of cell viability of BV-2 microglia cells damaged by nitric oxide. The groups treated with 5 and 50 mg/ml of Puerariae Radix demonstrated increases of cell viabilities of BV-2 microglia cells, but these were not significant statistically. These results suggested that Puerariae Radix revealed neuroprotective effects through the control effect of apoptosis and oxidative damages.

Neuroprotective and Anti-oxidant Effects of Gastrodiae Rhizoma Extracts against Hydrogen Peroxide-induced Cytotoxicity in SH-SY5Y Cells (산화적 스트레스에 대한 천마 추출물의 신경세포 보호 및 항산화 효과)

  • Kang Beom, Kwon;Ha Rim, Kim;Ye Seul, Kim;Eun Hee, Park;Han Byeol, Choi;Do Gon, Ryu
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.36 no.6
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    • pp.209-212
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    • 2022
  • We recently reported that Gastrodia elata extracts (GEE) had an effects to protect against lipopolysaccharide-induced cognitive impairment in vivo model. In this study, we investigated the neuroprotective effects and the mechanism of action of GEE in hydrogen peroxide (H2O2)-induced cell death of SH-SY5Y human neuroblastoma cell. The SH-SY5Y cells were divided into five groups, including control(non-treated group), 100 μM H2O2, 100, 200, 500 ㎍/㎖ GEE+ 100 μM H2O2 groups. Pre- and co-treatment with GEE prevented cell death induced by 100 μM H2O2 for 24 h in SH-SY5Y cells. Our findings also showed that anti-oxidants enzymes (Cu/Zn superoxide dismutase, Mn superoxide dismutase, catalase) were up-regulated by 100 μM H2O2. But GEE suppressed H2O2-induced anti-oxidants enzymes decrease in a dose-dependent manner. Treatment with GEE also inhibited phosphorylation of eukaryotic initiation factor-2α (eIF-2α) and p38 by H2O2. Taken together, the neuroprotective effects of GEE in terms of recovery of antioxidant enzymes expression, down-regulation of eIF-2α and p38 phosphorylation, and inhibition of cell death are associated with reduced oxidative stress in SH-SY5Y cells.

Neuroprotective Effects of Bunsimgieum (분심기음(分心氣飮)의 도파민 세포 보호 효과)

  • Kim, Ro-Sa;Lee, Chang-Hoon;Lee, Jin-Moo;Cho, Jung-Hoon;Jang, Jun-Bock;Lee, Kyung-Sub
    • The Journal of Korean Obstetrics and Gynecology
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    • v.22 no.2
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    • pp.119-131
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    • 2009
  • Purpose: The depression accompanied with menopuase shows the relation with the dopamine secretion. These studies were undertaken to evaluate the anti- oxidative and neuroprotective effects of Bunsimgieum(BSGE) on dopaminergic neurons. Methods: To estimate the antioxidant effects, we carried out 1.1-diphenyl-2- picrylhydrazyl (DPPH) free radical scavenging assay, 2,2'-azinobis-(3-ethylbenzothiazoline -6-sulfonic acid (ABTS) radical cation decolorization assay, and measurement of total polyphenolic content. To evaluate neuroprotective effect of BSGE in vitro, We performed thiazolyl blue tetrazolium bromide (MTT) assay, reactive oxygen species (ROS) creation in SH-SY5Y. Tyrosine hydroxylase (TH) immunocytochemistry, nitric oxide (NO) assay, and TNF-${\alpha}$ assay in primary rat mesencephalic dopaminergic neurons. Results: The DPPH free radical and the ABTS radical cation inhibition activities were increased at a dose dependent manner. Total polyphenolic content was 0.83%. In SH-SY5Y culture, BSGE significantly increased the decreased cell viability by 6-OHDA at the concentrations of 10${\mu}$g/m${\ell}$ in pre-treatment group, 0.1-200${\mu}$g/m${\ell}$ in post-treatment group. The production of ROS induced by 6-OHDA was significantly inhibited in BSGE treated group. In mesencephalic dopaminergic cell culture, the BSGE group reduced the dopaminergic cell loss against 6-OHDA toxicity and the production of No and TNF-${\alpha}$ at the concentration of 5${\mu}$g/m${\ell}$. Conclusion: These results shows that BSGE has antioxidant and neuroprotective effects in the dopaminergic cells through decreasing the production of ROS, NO and TNF-${\alpha}$ which can cause many neurodegenerative changes in brain cell. We suggest that BSGE could be useful for the treatment of postmenopausal depression related with the decrease of dopamine.

Neuroprotective Effects of Some Plant Extracts against Oxygen-Glucose Deprivation (OGD)-Induced Oxidative Cell Death on Neuronal Cell (산소-포도당 결핍(OGD) 유도성 신경세포 사멸에 대한 뇌 보호 효과를 가지는 수종 생약추출물의 검색)

  • Lee, Hak-Ju;Koo, Uk;Lee, Hyun-Jung;Lee, Dong-Ho;Mar, Woong-Chon
    • Korean Journal of Medicinal Crop Science
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    • v.17 no.5
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    • pp.341-345
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    • 2009
  • Cerebral ischemia results from a transient or permanent reduction in cerebral blood flow that decreases oxygen and glucose supply. When the cellular oxygen supply is reduced to critical level, damage to cells and induction of cell death are occurred by excitotoxicity, oxidative stress and inflammation. Ischemia remains one of the leading causes of death, but there is no effective treatment that might protect neurons gainst ischemia by interrupting the cascade of cell death. In this study, human neuroblastoma SH-SY5Y cells are exposed to oxygen and glucose deprivation (OGD) followed by reoxgenation. OGD can mimic the acute restriction of metabolite and oxygen supply caused by ischemia and is widely used as a model of ischemic conditions. SH-SY5Y cells are treated samples at the commencement of OGD to achieve different final concentrations, and cell viabilities were quantified using the measurement of flow cytometry analysis. Of those tested, the extracts of Polygala tenuifolia (roots), Dictamnus dasycarpus (barks), Polygala tenuifolia (roots), Eucommia ulmoides (branches), Eucommia ulmoides (barks), Poria cocos (whole), Sophora flavescens (roots) showed neuroprotective effects, with $EC_{50}$ values of $4.5{\pm}0.6$, $7.9{\pm}1.5$, $10.5{\pm}0.7$, $18.4{\pm}1.9$, $19.6{\pm}0.3$, $21.6{\pm}1.9$, and $30.7{\pm}3.9{\mu}g/m{\ell}$, respectively.

Phenolic Profiles of Hardy Kiwifruits and Their Neuroprotective Effects on PC-12 and SH-SY5Y Cells against Oxidative Stress

  • Jeong, Ha-Ram;Kim, Kwan Joong;Lee, Sang Gil;Cho, Hye Sung;Cho, Youn-Sup;Kim, Dae-Ok
    • Journal of Microbiology and Biotechnology
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    • v.30 no.6
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    • pp.912-919
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    • 2020
  • Hardy kiwifruits (Actinidia arguta Planch.) have high amounts of antioxidants, including ascorbic acid (vitamin C) and phenolics. The anti-cholinesterase activity and neuroprotective effects of three different cultivars of hardy kiwifruits, cv. Mansu (A. arguta × A. deliciosa), cv. Haeyeon (A. arguta), and cv. Chiak (A. arguta), on PC-12 and SH-SY5Y cells were evaluated. Extraction of phenolics and vitamin C was carried out using 80% (v/v) aqueous ethanol and metaphosphoric acid assisted with homogenization, respectively. Hardy kiwifruit of cv. Mansu showed higher total phenolic, total flavonoid, and vitamin C contents and antioxidant capacity compared to the other two cultivars of hardy kiwifruits, cv. Haeyeon and cv. Chiak. Analysis of high-performance liquid chromatography results revealed the presence of procyanidin B2, (-)-epicatechin, neochlorogenic acid, cryptochlorogenic acid, rutin, hyperoside, isoquercitrin, and astragalin in hardy kiwifruits. The three cultivars of hardy kiwifruits had a wide range of vitamin C content of 55.2-130.0 mg/100 g fresh weight. All three cultivars of hardy kiwifruits had protective effects on neuronal PC-12 and SH-SY5Y cells exposed to hydrogen peroxide by increasing cell viability and reducing intracellular oxidative stress. Furthermore, the hardy kiwifruits inhibited acetylcholinesterase and butyrylcholinesterase. Collectively, these results suggest that hardy kiwifruits rich in antioxidants like phenolics and vitamin C have good potential as functional materials in neuroprotective applications.