• Title, Summary, Keyword: neuroprotective effect

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Effect of Neurosteroid Modulation on Global Ischaemia-Reperfusion-Induced Cerebral Injury in Mice

  • Grewal, Amarjot Kaur;Jaggi, Amteshwar Singh;Rana, Avtar Chand;Singh, Nirmal
    • The Korean Journal of Physiology and Pharmacology
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    • v.17 no.6
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    • pp.485-491
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    • 2013
  • The present study was designed to investigate the putative effect of neurosteroid modulation on global ischaemia-reperfusion-induced cerebral injury in mice. Bilateral carotid artery occlusion followed by reperfusion, produced a significant rise in cerebral infarct size along with impairment of grip strength and motor coordination in Swiss albino mice. Administration of carbamazepine (16 mg/kg, i.p.) before global cerebral ischaemia significantly attenuated cerebral infarct size and improved the motor performance. However, administration of indomethacin (100 mg/kg, i.p.) attenuated the neuroprotective effect of carbamazepine. Mexiletine (50 mg/kg, i.p.) did not produce significant neuroprotective effect. It may be concluded that the neuroprotective effect of carbamazepine may be due to increase in synthesis of neurosteroids perhaps by activating enzyme ($3{\alpha}$ HSD) as indomethacin attenuated the neuroprotective effect of carbamazepine. The sodium channel blocking effect of carbamazepine may not be involved in neuroprotection as mexiletine, a sodium channel blocker, did not produce significant neuroprotective effect.

Testosterone-mediated Neuroprotection in NO Induced Cell Death of Motor Neuron Cells Expressing Wild Type or Mutant Cu/Zn Superoxide Dismutase (Cu/Zn Superoxide Dismutase 유전자 발현 운동신경세포주에서 NO 독성에 대한 Testosterone의 보호효과)

  • Kim, Nam Hee;Kim, Hyun Jung;Kim, Manho;Park, Kyung Seok;Lee, Kwang-Woo
    • Annals of Clinical Neurophysiology
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    • v.8 no.1
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    • pp.63-70
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    • 2006
  • Background: Testosterone is reported to have neuroprotective effect in various neurological diseases. Recently, the mechanism involved in nitric oxide (NO)-mediated motor neuron death is under extensive investigation. The Cu/Zn-superoxide dismutase (SOD1) mutations has been implicated in selective motor neuron death of amyotrophic lateral sclerosis (ALS) and it is said to play an important role in NO-mediated motor neuron death. However, neuroprotective effect of testosterone on motor neuron exposed to NO has rarely been studied. Methods: Motor neuron-neuroblastoma hybrid cells expressing wild-type or mutant (G93A or A4V) SOD gene were treated with $200{\mu}M$ S-nitrosoglutathione. After 24 hr, cell viability was measured by MTT assay. To see the neuroprotective effect of testosterone, pretreatment with 1 nM testosterone was done 1 hr before S-nitroglutathione treatment. To study the mechanism of protective effect, $20{\mu}M$ flutamide (androgen receptor antagonist) was also pretreated with testosterone 1 hr before S-nitroglutathione treatment. Results: S-nitrosoglutathione showed significant neurotoxic effect in all three cell lines. Percentage of cell death was somewhat different in each cell line. 1 nM testosterone showed neuroprotective effect in G93A and wild-type cell line. In A4V cell line, testosterone did not showed neuroprotective effect. The neuroprotective effect of testosterone was reversed by $20{\mu}M$ flutamide. Conclusions: These results indicate that testosterone induces neuroprotection in NO-mediated motor neuron death directly through the androgen receptor. This neuroprotective effect of testosterone varies according to the types of SOD1 gene mutation. These data suggest that testosterone may be of therapeutic value against ALS.

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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.

Neuroprotective Effect of Duloxetine on Chronic Cerebral Hypoperfusion-Induced Hippocampal Neuronal Damage

  • Park, Jin-A;Lee, Choong-Hyun
    • Biomolecules & Therapeutics
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    • v.26 no.2
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    • pp.115-120
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    • 2018
  • Chronic cerebral hypoperfusion (CCH), which is associated with onset of vascular dementia, causes cognitive impairment and neuropathological alterations in the brain. In the present study, we examined the neuroprotective effect of duloxetine (DXT), a potent and balanced serotonin/norepinephrine reuptake inhibitor, on CCH-induced neuronal damage in the hippocampal CA1 region using a rat model of permanent bilateral common carotid arteries occlusion. We found that treatment with 20 mg/kg DXT could attenuate the neuronal damage, the reduction of phosphorylations of mTOR and p70S6K as well as the elevations of $TNF-{\alpha}$ and $IL-1{\beta}$ levels in the hippocampal CA1 region at 28 days following CCH. These results indicate that DXT displays the neuroprotective effect against CCH-induced hippocampal neuronal death, and that neuroprotective effect of DXT may be closely related with the attenuations of CCH-induced decrease of mTOR/p70S6K signaling pathway as well as CCH-induced neuroinflammatory process.

Protective Effect of Extracts from Euryale ferox against Glutamate-induced Cytotoxicity in Neuronal Cells

  • Lee, Mi-Ra;Kim, Ji-Hyun;Son, Eun-Soon;Park, Hae-Ryong
    • Natural Product Sciences
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    • v.15 no.3
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    • pp.162-166
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    • 2009
  • Oxczaasssaidative stress plays an important role in neuronal cell death, which is associated with neurodegenerative conditions such as Alzheimer's and Parkinson's disease. This study evaluated the neuroprotective effect of Euryale ferox (EF) extracts against glutamate-induced cytotoxicity in hybridoma N18-RE-105 cells. Specifically, neuroprotective effects of methanol and ethanol extracts were evaluated by the MTT reduction assay. The ethanol extracts of EF displayed dose dependent protection against neuronal cell death induced by 20 mM of glutamate. Furthermore, the ethanol extracts of EF was sequentially fractionated with hexane, diethyl ether, ethyl acetate, and water layer according to degree of polarity. The hexane fractions exhibited neuroprotective effect against glutamate-stressed N18-RE-105 cells. Overall, results suggest that EF extracts can potentially be used as chemotherapeutic agents against neuronal diseases.

Neuroprotective Effect of Visnagin on Kainic Acid-induced Neuronal Cell Death in the Mice Hippocampus

  • Kwon, Min-Soo;Lee, Jin-Koo;Park, Soo-Hyun;Sim, Yun-Beom;Jung, Jun-Sub;Won, Moo-Ho;Kim, Seon-Mi;Suh, Hong-Won
    • The Korean Journal of Physiology and Pharmacology
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    • v.14 no.5
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    • pp.257-263
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    • 2010
  • Visnagin (4-methoxy-7-methyl-5H-furo[3,2-g][1]-benzopyran-5-one), which is an active principle extracted from the fruits of Ammi visnaga, has been used as a treatment for low blood-pressure and blocked blood vessel contraction by inhibition of calcium influx into blood cells. However, the neuroprotective effect of visnagin was not clearly known until now. Thus, we investigated whether visnagin has a neuroprotective effect against kainic acid (KA)-induced neuronal cell death. In the cresyl violet staining, pre-treatment or post-treatment visnagin (100 mg/kg, p.o. or i.p.) showed a neuroprotective effect on KA ($0.1{\mu}g$) toxicity. KA-induced gliosis and proinflammatory marker (IL-$1{\beta}$, TNF-${\alpha}$, IL-6, and COX-2) inductions were also suppressed by visnagin administration. These results suggest that visnagin has a neuroprotective effect in terms of suppressing KA-induced pathogenesis in the brain, and that these neuroprotective effects are associated with its anti-inflammatory effects.

Two Neuroprotective Compounds from Mushroom Daldinia concentrica

  • Lee, In-Kyoung;Yun, Bong-Sik;Kim, Young-Ho;Yoo, Ick-Dong
    • Journal of Microbiology and Biotechnology
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    • v.12 no.4
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    • pp.692-694
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    • 2002
  • In the course of our screening for neuroprotective agents, a new compound (1) was isolated together with a known compound, caruilignan C (2), from the fruiting body of Daldinia concentrica. Their structures were determined on the basis of various spectral studies. Both compounds exhibited neuroprotective effect against iron-induced neurodegeneration in a primary culture of mouse cortical neurons.

The Neuroprotective Effects of Carnosine in Early Stage of Focal Ischemia Rodent Model

  • Park, Hui-Seung;Han, Kyung-Hoon;Shin, Jeoung-A;Park, Joo-Hyun;Song, Kwan-Young;Kim, Doh-Hee
    • Journal of Korean Neurosurgical Society
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    • v.55 no.3
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    • pp.125-130
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    • 2014
  • Objective : This study was conducted to elucidate neuroprotective effect of carnosine in early stage of stroke. Methods : Early stage of rodent stroke model and neuroblastoma chemical hypoxia model was established by middle cerebral artery occlusion and antimycin A. Neuroprotective effect of carnosine was investigated with 100, 250, and 500 mg of carnosine treatment. And antioxidant expression was analyzed by enzyme linked immunosorbent assay (ELISA) and western blot in brain and blood. Results : Intraperitoneal injection of 500 mg carnosine induced significant decrease of infarct volume and expansion of penumbra (p<0.05). The expression of superoxide dismutase (SOD) showed significant increase than in saline group in blood and brain (p<0.05). In the analysis of chemical hypoxia, carnosine induced increase of neuronal cell viability and decrease of reactive oxygen species (ROS) production. Conclusion : Carnosine has neuroprotective property which was related to antioxidant capacity in early stage of stroke. And, the oxidative stress should be considered one of major factor in early ischemic stroke.

Neuroprotective effects of Sohaphwangwon essential oil in a Parkinson's disease mouse model (MPTP로 유도된 Parkinson's disease 동물 모델을 이용한 소합향원(蘇合香元)의 신경보호 효과 및 그 작용 기전 연구)

  • Kim, In-Ja;Lee, Ji-Hyun;Song, Kyoo-Ju;Koo, Byung-Soo;Kim, Geun-Woo
    • Journal of Oriental Neuropsychiatry
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    • v.23 no.1
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    • pp.129-143
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    • 2012
  • Objectives : To evaluate the neuroprotective effects of the essential oil from Sohaphwangwon (SH), a Chinese traditional medicinal prescription in a Parkinson's disease mouse model. Methods : 1. The neuroprotective effect of SH on primary neuronal cells was examined by using 1-methyl-4-phenylpyridinium ion (MPP+). 2. The neuroprotective effect of SH was examined in a Parkinson's disease mouse model. C57BL/6 mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 30 mg/kg/day), intraperitoneal (i.p.) for 5 days. SH inhalation was applied before MPTP treatment for 7 days and continued until 12 days after the first MPTP treatment. 3. To find out the intracellular target signal molecule(s) regarding the neuroprotective effect of SH essential oil, brain-derived neurotropic factor (BDNF) and synaptic protein SNAP25 were examined by Western blot analysis. Results : 1. MPP+ induced a concentration-dependent decrease in cell viability. However, in the presence of 3 and 5 ug/ml of SH, MPP+-induced cell death was significantly reduced. 2. SH inhalation in MPTP mice led to the restoration of behavioral impairment and rescued tyrosine hydroxylase (TH)-positive dopaminergic neurodegeneration. 3. In SH / MPTP mice, BDNF and SNAP25 increased. Conclusions : This experiment suggests that the neuroprotective effect of SH essential oil is mediated by the expression of BDNF. Furthermore, SH essential oil may serve as a potential preventive or therapeutic agent regarding Parkinson's disease.

Neuroprotective Effect of HyulBuChookAu-Tang on Focal Cerebral Ischemia of the Rats

  • Cho Eun-Hee;Kim Young-Gyun;Kwon Jung-Nam
    • The Journal of Korean Medicine
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    • v.27 no.2
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    • pp.70-85
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    • 2006
  • Objectives; This study examined the neuroprotective effect of Hyulbuchookautang (血府逐瘀湯, HBCAT)against neural damage following focal cerebral infarction. Methods : Sprague-Dawley Rats were induced with focal cerebral infarction by temporal middle cerebral artery occlusion (MCAO). The rats were divided into 2 groups. We treated extract of HBCAT to one group after operation (sample group), and the other group wasn't treated after operation (control group). We observed neurological scores and TIC-stained infarct area, total infarct volume in brain sections and Bax-positive neurons, HSP70- positive neurons in brain regions. Results : HBCAT treatment at 3 days after MCAO reduced neurological scores induced by MCAO. HBCAT treatment at 5 days after MCAO reduced TTC-stained infarct area in brain sections induced by MCAO. HBCAT treatment at 5 days after MCAO reduced total infarct volume in brain sections induced by MCAO. HBCAT treatment after MCAO reduced Bax-positive neurons in cortex infarct core and cortex infarct penumbra and caudo-putamen of brain regions induced by MCAO. HBCAT treatment after MCAO reduced HSP70- positive neurons in cortex infarct penumbra of brain regions induced by MCAO. Conclusions : These results suggest that HBCAT has a neuroprotective effect against focal cerebral ischemia.

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