• Title/Summary/Keyword: neuronal cell protection

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Tyrosinase Inhibitory Activity and Neuronal Cell Protection of Hydrothermal Extracts from Watermelons (수박 열수 추출물의 Tyrosinase 저해능과 신경세포 보호효과)

  • Heo, Da-Jeong;Kim, Su-Jung;Choi, Ae-Ran;Park, Hae-Ryong;Lee, Seung-Cheol
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.42 no.10
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    • pp.1707-1711
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    • 2013
  • In our study, each part (flesh, white rind, and green rind) of watermelon was extracted using hydrothermal extraction method at temperatures ranging from 100 to $300^{\circ}C$ at the intervals of 10, 30, and 60 min. We found that hydrothermal treatment has a significant bearing not only on tyrosinase inhibitory activity but also on neuronal cell protection of watermelon parts. The peak tyrosinase inhibitory activity (about 93%) was observed in both the flesh and green rind extracts at $300^{\circ}C$ for 60 min. In addition, we observed that hydrothermal extracts of watermelon parts at $300^{\circ}C$ for 60 min also evidenced significant protection effect for neuronal cell against $H_2O_2$ in a concentrationdependent manner. The results of this study confirm that hydrothermal treatment may be an efficient processing method for the purpose of obtaining potent bioactive substances from watermelon.

Screening of 56 Herbal formulas covered by the National Health Insurance Service on Dementia-related Factors (국민 건강보험 급여 한약 처방 56종의 치매 주요 생리지표 및 신경세포 변화에 대한 효능 비교 연구)

  • Lim, Hye-Sun;Kim, Yu Jin;Kim, Yoon ju;Kim, Bu-Yeo;Jeong, Soo-Jin
    • The Journal of Korean Medicine
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    • v.39 no.3
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    • pp.1-16
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    • 2018
  • Objectives: The purpose of this study was to investigate the effects of 56 herbal formulae covered by the National Health Insurance Corporation (NHIC) on dementia-related biomarkers and neuronal cell changes. Methods: The 56 herbal formulae were extracted with 70% ethanol at $100^{\circ}C$ for 2 h. The antioxidant properties was measured by radical scavenging assay using ABTS+ radical. The acetylcholinesterase (AChE) activity was tested by Ellman's assay and $amyloid-{\beta}$ ($A{\beta}$) aggregation was determined using fluorescence method. To estimate the inhibitory effects of herbal formulae on neuronal cell death and inflammation using HT22 hippocampal cells and BV-2 microglia, respectively. Results: Among the 56 herbal formulae, Dangguiyukhwangtang, Banhasasimtang, Samhwangsasimtang, Cheongwiesan, Hwangryunhaedoktang, Banhabaekchulchunmatang, Jaeumganghwatang, Cheongseoikgitang, and Hoechunyanggyuksan has a significant inhibitory effects on acetylcholinesterase (AChE) activity. Doinseunggitang and Samhwangsasimtang exerted the effect on the inhibition of $amyloid-{\beta}$ ($A{\beta}$) aggregation. Additionally, 10 herbal formulae affected AChE and $A{\beta}$ aggregation revealed antioxidant activity as well as neuroprotective and anti-neuroinflammation effects in neuronal cell lines. Conclusions: 10 herbal formulae that have been shown to be effective against the major dementia markers have been shown to have antioxidant activity, neuronal cell protection and inhibition of brain inflammation. Further investigation of these herbal formulae will need to be validated in dementia animal models.

Effects of Sokmyeung-tang(SMT) on the Protection of C6 Glial Cells and Ischemic Brain Damage (속명탕(續命湯)이 C6 glial cell 보호 및 허혈성 뇌손상에 미치는 영향)

  • An, Ga-Yong;Choi, Eun-Hee;Kim, In-Soo;Kang, Seong-Sun;Lee, Young-Soo;Hong, Seok;Jeon, Sang-Yun
    • The Journal of Internal Korean Medicine
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    • v.32 no.1
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    • pp.43-55
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    • 2011
  • Objectives : Sokmyeung-tang(SMT) has been used for treatment of CVA in traditional oriental medicine, so this study was designed to evaluate the effect of SMT's protection on brain cell damage against the oxidative stress that was affected by CVA, We also investigated the effect of motor function improvement and neurotrophic factor in ischemic cerebral damaged rats. Methods : We measured cell viability after administrating SMT, chemicals(Paraquat, SNP, rotenone, and $H_2O_2$) which cause oxidative stress, and both SMT and chemicals. We carried out neurobehavioral evaluation(Rotarod test, Beam-walking test, postural reflex test) and observed BDNF (brain-derived neurotrophic factor) expression by injecting SMT into ischemic cerebral damaged rat. Results : Through this study, we observed the following three results. First, brain cell death caused by paraquat, rotenone, and $H_2O_2$ significantly decreased with the treatment of SMT. Second, neuronal movement function in ischemic cerebral damaged rats was significantly improved by the treatment of SMT. Third, BDNF in ischemic cerebral damaged rats increased with the treatment of SMT. Conclusions : SMT protects brain cells from damage induced by oxidative stress (Paraquat, rotenone, $H_2O_2$). SMT also improves neuronal movement function and increases BDNF in ischemic cerebral damaged rats.

Effect of Korea Red Ginseng Extract on PC12 Cell Death Induced by Serum Deprivation (홍삼 수용성 추출물이 PC12 세포사멸에 미치는 영향)

  • Lee, Sang-Hyun;Yun, Young-Gab
    • Journal of Korean Medicine Rehabilitation
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    • v.19 no.2
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    • pp.103-112
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    • 2009
  • Objectives : This study was to evaluate the pharmacological effect of Korea Red Ginseng aqueous extract (KRGE) on serum-deprived apoptosis of neuronal-like pheochromocytoma PC12 cells and to investigate its underlying action mechanism. Methods : KRGE was prepared by extracting Korea Red Ginseng with hot water and concentrating using a vacuum evaporator. Cell viability was determined after incubation of cells with KRGE or chemical inhibitor in serum-deprived medium for 60 h by counting intact nuclei following lysing of the cell membrane. Caspase activities were measured using chromogenic substrates and signal-associated protein phosphorylation and cytochrome c release were determined by Western blot analyses using their specific antibodies. Results : Serum deprivation induced PC12 cell death, which was accompanied by typical morphological features of apoptotic cell, such as nuclear fragmentation, caspase-3 activation, and cytochrome c release. This apoptotic cell death was significantly inhibited by KRGE and caspase-3 inhibitor, but not by the addition of NMA, ODQ, and PD98059. KRGE promoted phosphorylation of Akt and Bad, and this phosphorylation was inhibited by the PI3K inhibitor LY92004. In addition, this inhibitor also reversed KRGE-mediated protection of PC 12 cells from serum deprivation. These results suggested that KRGE protects PC12 cells from serum deprivation-induced apoptosis through the activation of PI3K/Akt-dependent Bad phosphorylation and cytochrome c release, resulting in caspase-3 activation. Conclusions : KRGE should be considered as a potential therapeutic drug for brain diseases including stroke induced by apoptosis of neuronal cells.

Effect of Chungpaesagan-tang on Ischemic Damage in Organotypic Hippocampal Slice Culture (청폐사간탕(淸肺瀉肝湯)이 뇌해마 조직배양의 신경세포 자연사에 미치는 영향)

  • Lee, Min-Young;Ku, Ja-Seung;Kim, Sung-Hoon;Kim, Yoon-Bum;Kim, Sun-Yeou;Choi, Hyeon;Sohn, Young-Joo;Jung, Hyuk-Sang;Sohn, Nak-Won
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.22 no.4
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    • pp.771-777
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    • 2008
  • Chungpaesagan-tang which is used for treating patients of brain in cerebrovascular disease frequently from clinical doctor has not reported about the effect of neuronal aptosis caused of brain ischemia. The aim of this study is to investigate effect of Chungpaesagan-tang protecting neuronal cells from being damaged by brain ischemia through using organotypic hippocampal slice cultures. We caused ischemic damage to organotypic hippocampal slice cultures by oxygen and glucose deprivation. And added Chungpaesagan-tang extract to cultures. thereafter we measured area percentage of propidium iodide (PI)-stained neuronal cell, lactate dehydrogenase (LDH) levels in culture media and Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells. Area percentage of PI-stained neuronal cells and count of TUNEL-positive cells in CA1 and DG area of organotypic hippocampal slice culture were significantly decreased in pertinent density level of Chungpaesagan-tang extract. LDH levels in culture media of organotypic hippocampal slice culture were significantly decreased in pertinent density level of Chungpaesagan-tang extract. Within pertinent density level, Chungpaesagan-tang has cell protection effect that prevents brain ischemia damaging neuronal cells and apoptosis increasing.

The effects of nutrient depleted microenvironments and delta-like 1 homologue (DLK1) on apoptosis in neuroblastoma

  • Kim, Yu-Ri
    • Nutrition Research and Practice
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    • v.4 no.6
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    • pp.455-461
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    • 2010
  • The tumor microenvironment, particularly sufficient nutrition and oxygen supply, is important for tumor cell survival. Nutrition deprivation causes cancer cell death. Since apoptosis is a major mechanism of neuronal loss, we explored neuronal apoptosis in various microenvironment conditions employing neuroblastoma (NB) cells. To investigate the effects of tumor malignancy and differentiation on apoptosis, the cells were exposed to poor microenvironments characterized as serum-free, low-glucose, and hypoxia. Incubation of the cells in serum-free and low-glucose environments significantly increased apoptosis in less malignant and more differentiated N-type IMR32 cells, whereas more malignant and less differentiated I-type BE(2)C cells were not affected by those treatments. In contrast, hypoxia (1 % $O_2$) did not affect apoptosis despite cell malignancy. It is suggested that DLK1 constitutes an important stem cell pathway for regulating self-renewal, clonogenicity, and tumorigenicity. This raises questions about the role of DLK1 in the cellular resistance of cancer cells under poor microenvironments, which cancer cells normally encounter. In the present study, DLK1 overexpression resulted in marked protection from apoptosis induced by nutrient deprivation. This in vitro model demonstrated that increasing severity of nutrition deprivation and knock-down of DLK1 caused greater apoptotic death, which could be a useful strategy for targeted therapies in fighting NB as well as for evaluating how nutrient deprived cells respond to therapeutic manipulation.

Neuronal Cell Protection and Antioxidant Activities of Hot Water Extract from Commercial Buckwheat Tea (시판 메밀차 열수 추출물의 항산화 및 신경세포 보호효과)

  • Jeong, Chang-Ho;Jeong, Hee-Rok;Choi, Sung-Gil;Shim, Ki-Hwan;Heo, Ho-Jin
    • Food Science and Preservation
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    • v.18 no.3
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    • pp.358-365
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    • 2011
  • The antioxidant and neuronal cell-protective effects of hot water extract from commercial buckwheat tea (CBTE) were evaluated. The 2,2'-azino-bis(3-ethyl-benzthiazoline-6-sulfonic acid) (ABTS) radical scavenging activity, ferric reducing antioxidant power (FRAP), and malondialdehyde (MDA) inhibitory effect of the CBTE increased in a dose-dependent manner. The Intracellular reactive oxygen species (ROS) accumulation that resulted from hydrogen peroxide ($H_2O_2$) treatment more significantly decreased when CBTE was present in the media than when the PC12 cells were treated only with $H_2O_2$. In the neuronal cell viability assay using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazoliumbromide (MTT), the aqueous extracts showed a protective effect against $H_2O_2$-induced neurotoxicity, and the lactate dehydrogenase (LDH) release into the medium was also inhibited by CBTE. The total phenolics of CBTE was 9,608.10 mg/100 g, and the major phenolic compounds were rutin (13.42 mg/100 g) and quercitrin (0.90 mg/100 g). These data suggested that CBTE, including the aforementioned phenolics, may be useful in reducing the risk of neurodegenerative disease.

Protective Effects of Seok-Jeong on the Toxicity of Cadmium in Neuronal Cells (뇌신경세포에서 토양미생물 발효추출액인 석정의 카드뮴 독성에 대한 방어효과)

  • 홍순해;안성희;장봉기;박종안;이종화
    • YAKHAK HOEJI
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    • v.47 no.2
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    • pp.85-92
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    • 2003
  • Seok-jeong (SJ) is a solution of various metal ions and numerous other organic substances produced through extraction and fermentation of herbs and soil using geo-microbes, and it has been shown to improve symptoms of senile dementia. In this study, we investigated the protective effects of SJ against neurotoxicity of cadmium in HT22 hippocampal neuron cell line. SJ significantly protected from the cadmium-induced decreased cell viability measured by MTT assay (p<0.01). The protective effects of SJ against cadmium toxicity were confirmed through observing morphological changes using inverted microscope. Additionally, SJ significantly repressed the formation of lipid peroxidation induced by high concentration of cadmium, and likewise, significantly repressed the reduction of glutathione by cadmium in HT22 cells. Vitamin C at the concentration found in SJ did not show any protective effect against cadmium toxicity in HT22 cells, indicating that vitamin C may not have a major role in the protective mechanism of SJ. Taken together, these results suggest that SJ may be a valuable agent for the protection of cadmium toxicity on the neuronal cells, and that the mechanism of the action of SJ may be due to reduced lipid peroxidation and increased glutathione level.

Antioxidative Role of Selenoprotein W in Oxidant-Induced Mouse Embryonic Neuronal Cell Death

  • Chung, Youn Wook;Jeong, Daewon;Noh, Ok Jeong;Park, Yong Hwan;Kang, Soo Im;Lee, Min Goo;Lee, Tae-Hoon;Yim, Moon Bin;Kim, Ick Young
    • Molecules and Cells
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    • v.27 no.5
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    • pp.609-613
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    • 2009
  • It has been reported that selenoprotein W (SelW) mRNA is highly expressed in the developing central nerve system of rats, and its expression is maintained until the early postnatal stage. We here found that SelW protein significantly increased in mouse brains of postnatal day 8 and 20 relative to embryonic day 15. This was accompanied by increased expression of SOD1 and SOD2. When the expression of SelW in primary cultured cells derived from embryonic cerebral cortex was knocked down with small interfering RNAs (siRNAs), SelW siRNA-transfected neuronal cells were more sensitive to the oxidative stress induced by treatment of $H_2O_2$ than control cells. TUNEL assays revealed that $H_2O_2$-induced apoptotic cell death occurred at a higher frequency in the siRNA-transfected cells than in the control cells. Taken together, our findings suggest that SelW plays an important role in protection of neurons from oxidative stress during neuronal development.