• Monthly Korean Chicken
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• v.15 no.1
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• pp.92-93
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• 2009

성인의 하루 섭취 열량은 대략 2,000㎉ 로, 이중 약 20%는 뇌에서 소비한다. 뇌에는 1,000억 개가 넘는 신경세포가 있는데, 이 세포들이 제대로 기능하기 위 해서는 생각보다 많은 에너지가 필요하다. 이와 관련해 현대인들의 우울증의 원인을 식습관에서 찾는 견해도 있다. 균형이 맞지 않는 식습관 때문에 뇌가 활력을 잃어 멍하고 무기력한 상태가 되는 경우를 우울증으로 판단하는 경우가 적지 않기 때문이다. 그렇다면 식습관만 제대로 바꿔도 가벼운 우울증은 금방 나을 수 있게 될 것이다. 일본의 대중지'주간 겐다이'는 최근호에서 약학 전문가 이쿠타 사토시 박사의 의견을 빌어 뇌에 활력을 주는 식품을 소개했다.

• Journal of the korean academy of Pediatric Dentistry
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• v.33 no.1
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• pp.13-24
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• 2006

Neuronal apoptotic events, consequently resulting in neuronal cell death, are occurred in hypoxic/ischemic condition. This cell death has been shown to be accompanied with the production of reactive oxygen species (ROS), which can attack cellular components such as nucleic acids, proteins and phospholipid. However, the underlying mechanisms of apoptosis induced in hypoxic/ischemic condition and its treatment methods are unsettled. Cobalt chloride $(CoCl_2)$ has been known to mimic hypoxic condition including the production of ROS. Epigallocatechin gallate (EGCG), a green tea polyphenol, has diverse pharmacologial activities in cell growth and death. This study was aimed to investigate the apoptotic mechanism by $CoCL_2$ and effects of EGCG on $CoCl_2-induced$ apoptosis in PC12 cells. Administration of $CoCl_2$ decreased cell survival in dose- and time-dependent manners and induced genomic DNA fragmentation. Treatment with $100{\mu}M$ EGCG for 30 min before PC12 cells were exposed to $150{\mu}M$ $CoCl_2$, being resulted in the cell viability and DNA fragmentation being rescued. $CoCl_2$ caused morphologic changes such as cell swelling and condensed nuclei whereas EGCG attenuated morphologic changes by $CoCl_2$. EGCG suppressed the apoptotic peak and a loss of ${\Delta}{\psi}_m$ induced by $CoCl_2$. $CoCl_2$ decreased Bcl-2 expression but Bax expression was not changed in $CoCl_2$- treated cells. EGCG attenuated the Bcl-2 underexpression by $CoCl_2$. $CoCl_2$ augumented the cytochrome c release from mitochondria into cytoplasm and increased caspase-8, -9 and caspase-3 activity a marker of the apoptotic executing stage. EGCG ameliorated the incruement in caspase-8, -9 and -3 activity, and cytochrome c release by $CoCl_2$ NAC (N-acetyl-cysteine), a scavenger of ROS, attenuated $CoCl_2-induced$ apoptosis in consistent with those of EGCG. These results suggest that $CoCl_2$ induces apoptotic cell death through both mitochondria- and death receptor-dependent pathway and EGCG has neuroprotective effects against $CoCl_2-induced$ apoptosis in PC12 cells.

• Journal of the korean academy of Pediatric Dentistry
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• v.28 no.4
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• pp.709-727
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• 2001

The pattern of programmed cell death(PCD) has been examined during the early developmental period of development in mouse embryos, from embryonic day 4.5(E4.5) to E11.5 Embryos from Balb/c breedings were harvested at various embryonic stages between E4.5 and El1.5. Cell death was analysed by in situ terminal deoxynucleotidyl transferase mediated dUTP nick end labeling(TUNEL) staining in tissue sections and whole embryos. At the blastocyst stage(E4.5), a very few apoptotic cells were found in the inner cell mass of the blastocyst. In the early egg cylinder stage(35.0-5.5), a few apoptotic cells were detected in the embryonic ectoderm, the embryonic endoerm and the proamniotic cavity. In the advanced egg cylinder stage(E5.5-6.5), TUNEL-posifive cells were observed in the extra-embryonic ectoderm and extra-embryonic endoderm as well as in the embryonic ectoderm, embryonic visceral endoderm and proamniotic cavity. In the streak stage(E6.75-7.75), many TUNEL-positive cells were found in the ectoplacental cone. In contrast, only very few apoptotic cells were found in the chorion and extra-embryonic endoderm in extra-embryonic regions. In intra-embryonic region, a few apoptotic cells were randomly found in the embryonic ectoderm, mesoderm and visceral endoderm. At the early somitogenesis stage(E8.0-8.5), most apoptotic cells were observed in the most cranial portion of neural fold (neural ectoderm and adjacent ectoderm). At the mid somitogenesis stage(39.0-9.5), the otic placode first showed TUNEL-positive at this stage. Small number of TUNEL-positive cells were also first seen around optic placode and branchial arches. Three streams of TUNEL-positive cells were clearly seen in the cranial region at 59.5-9.75. At E10.5, apoptotic cells were localized in the developing eye, the junctional portion of medial nasal, lateral nasal and maxillary processes, the lateral portion of branchial arches, the junction of bilateral mandibular processes, and apical ectodermal ridges of limb buds. At E11.5, apoptotic cells were noticeably decreased in most area, except the developing limbs and several somites in the tail region. In this study, the global temporospatial pattern of PCD throughout early development of mouse embryos was discussed. It may provide the basis for further studies on its role in the morphogenesis of the embryo.

• Journal of Life Science
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• v.32 no.10
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• pp.771-777
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• 2022

Dopaminergic (DA) cell death in Parkinson's disease (PD) has been attributed to multiple, distinct genetic and environmental factors. In rare familial PD loss of parkin function mutations play a key role in nigral DA neuron-specific pathogenesis primarily via endoplasmic reticulum (ER) stress. In more prevalent sporadic PD, environmental exposure to pesticides has a significant epidemiological role. However, it is largely unknown how environmental exposure to xenobiotics is etiologically linked with the known etiology in familial PD. In the present study biochemical evidence for a common pathogenic mechanism between sporadic and familial PD has been identified employing the recently characterized mesencephalic DA cell line, N27-A. Dieldrin, an organochlorine pesticide epidemiologically implicated in sporadic PD, induced the markers of ER stress response such as a chaperone BiP/Grp78, heme oxygenase-1 and especially, parkin. Accordingly, dieldrin activated the ER resident Caspase-12, a mediator of ER stress-specific apoptosis, during cell death of N27-A cells. Of great interest the dieldrin-induced DA neuronal cell death was synergistically rescued by the overexpression of ER resident neuroprotective proteins, parkin and Bcl-2. The present findings implicate that accumulation of ER stress could be one of common pathogenic mechanisms in idiopathic and familial PD, and some ER proteins, such as parkin and Bcl-2 may effectively attenuate ER stress-mediated N27-A DA cell death.

• Journal of the Korean Society of Food Science and Nutrition
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• v.41 no.8
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• pp.1072-1078
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• 2012

The potential antioxidant and anti-inflammatory effect of water and ethanol extracts from Flammulina velutipes (Curtis) Singer (FVS) on hydrogen peroxide ($H_2O_2$) and LPS-induced oxidative damage in PC-12 and RAW264.7 cells were investigated. The DPPH radical scavenging activities of the water extract from FVS was the highest, and the 50% inhibitory concentration value was 0.388 mg/mL. Also, the antioxidant activities of water and ethanol extracts were determined by ferric reducing antioxidant power, 2,2'-azino-bis-(3-ethybenzothiazoline-6-sulphonic acid) radical scavenging activity. In addition, water extract from FVS showed a strongly inhibitory effect on lipid peroxidation by measuring ferric thiocyanate values. The water extract decreased cell apoptosis in PC-12 cells against $H_2O_2$-induced oxidative damage. In addition, FVS extracts exhibited the strongest nitric oxide (NO) inhibition activity. It was also found that FVS extract inhibited LPS-induced iNOS and COX-2 expression in RAW264.7 cells. The findings of the present study suggest that extracts of FVS exhibit anti-oxidative and anti-inflammatory activity against oxidative stress and/or stimulated cells.

• Food Science and Preservation
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• v.14 no.2
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• pp.213-219
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• 2007

To develop an anti-dementia agent with potential therapeutic value in the protection of neuronal cells, we selected a water extract of Helianthus annuus seed for analysis. We measured acetylcholinesterase inhibitory activity in the extract, and analyzed the protective effect of the extract on neuronal cell death induced by hydrogen peroxide, or amyloid ${\beta}-peptide$, of SH-SY5Y neuroblastoma cells. The result showed that the extinct exerted protective effects of 83%, 72% and 53% respectively, on cell death induced by 100M, 200M, and 500M hydrogen peroxide. Also, when 50M of amyloid ${\beta}-peptide$ was added to the cells, the extract showed a protective effect (up to 80%) on cell death. Overall, the results showed that the H. annuus extract inhibited acetylcholinesterase activity in a dose-dependent manner, and the extract also strongly protected against cell death induced by hydrogen peroxide or amyloid ${\beta}-peptide$.

• Clinical and Experimental Pediatrics
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• v.52 no.12
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• pp.1337-1347
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• 2009

Purpose:Taurine (2-aminoethanesulfonic acid) is a simple sulfur-containing amino acid. It is abundantly present in tissues such as brain, retina, heart, and skeletal muscles. Current studies have demonstrated the neuroprotective effects of taurine, but limited data are available for such effects during neonatal period. The aim of this study was to determine whether taurine could reduce hypoxic-ischemic (HI) cerebral injury via anti-apoptosis mechanism. Methods:Embryonic cortical neurons isolated from Sprague-Dawley (SD) rats at 18 days gestation were cultured in vitro. The cells were divided into hypoxia group, taurine-treated group before hypoxic insult, and taurine-treated group after HI insult. In the in vivo model, left carotid artery ligation was performed in 7-day-old SD rat pups. The pups were exposed to hypoxia, administered an injection of 30 mg/kg of taurine, and killed at 1 day, 3 days, 1 week, 2 weeks, and 4 weeks after the hypoxic insult. We compared the expressions of Bcl-2, Bax, and caspase-3 among the 3 groups by using real- time polymerase chain reaction (PCR) and western blotting. Results:The cells in the taurine-treated group before hypoxic insult, although similar in appearance to those in the normoxia group, were lesser in number. In the taurine-treated group, Bcl-2 expression increased, whereas Bax and caspase-3 expressions reduced. Conclusion:Taurine exerts neuroprotective effects onperinatal HI brain injury due to its anti-apoptotic effect. The neuroprotective effect was maximal at 1-2 weeks after the hypoxic injury.

• Journal of Oriental Neuropsychiatry
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• v.11 no.2
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• pp.1-9
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• 2000

In previous studies, heat shock has been reported to induce the apoptosis or programmed cell death through the activation of caspase-3. 1 investigated the effect of juniper pure essential oil on the heat shock-induced apoptosis in human astrocyte cell line CCF-STTGI. Treatment of the astrocytes with heat shock markedly induced apoptotic cell death. However, pretreatment of the astrocytes with juniper oil ingibited the heat shock-induced apoptosis. To determine whether juniper inhibits the heat shock-induced activation of these apoptotic proteases, activation of CPP32 was assessed by Western blotting. Consistent with flow cytometry. DNA fragmentation and giemsa staining, heat shock-induced activation of CPP32 was blocked by juniper oil. Poly(ADP-ribose) polymerase (PARP), cysteine protease substrates were fragmented as a consequence of apoptosis by heat shock. Juniper oil inhibited the PARP fragmentation. This juniper oil also inhibited the heat shock-induced activation of caspase-3. These results suggest that juniper oil may modulate the apoptosis through the activation of the interleukin-1-converting enzyme-like protease.

• Journal of Oriental Neuropsychiatry
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• v.11 no.1
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• pp.37-46
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• 2000

We investigated the effects of lemon pure essential oils on the heat shock-induced apoptosis in human astrocyte cell line CCF-STTG1. In previous studies, hear shock has been reported to induce the apoptosis or programmed cell death through the activation of caspase-3. Treatment of CCF-STTG1 cells with heat shock markedly induced apoptotic cell death as determined by flow cytometry. Interestingly, pretreatment of CCF-STTG1 cells with lemon pure essential oils inhibited the heat shock-induced apoptosis. Lemon also inhibited the heat shock-induced apoptosis in primary cultured rat astrocytes. To determine whether lemon inhibits the heat shock-induced activation of these apoptotic proteases, activation of CPP32 was assessed by Western blotting. Consistent with flow cytometry, DNA fragmentation and giemsa staining, heat shock-induced activation of CPP32 was blocked by lemon pure essential oil. PARP, cysteine protease substrates were fragmented as a consequence of apoptosis by heat shock. Lemon oil inhibited the PARP fragmentation. This essential oil also inhibited the heat shock-induced activation of caspase-3. These results suggest that lemon pure essential oils may modulate the apoptosis through the activation of the ICE-like caspases.

• Tuberculosis and Respiratory Diseases
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• v.56 no.2
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• pp.187-197
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• 2004

Background : Nitric Oxide (NO) is a multi-faceted molecule with dichotomous regulatory roles in many areas of biology. NO can promote apoptosis in some cells, whereas it inhibits apoptosis in other cell types. This study was performed to characterize NO-induced cell death in lung epithelial cells and to investigate the roles of cell death regulators including iron, bcl-2 and p53. Methods : A549 cells were used for lung epithelial cells. SNP (sodium nitroprusside) and SNAP (S-nitroso-N-acetyl- penicillamine) were used for NO donor. Cytoxicity assay was done by MTT assay and crystal violet assay. Apoptotic assay was done by fluorescent microscopy after double staining with propidium iodide and hoecst 33342. Iron inhibition study was done with RBCs and FeSO4. For bcl-2 study, bcl-2 overexpressing cells (A549-bcl-2) were used and for p53 study, Western blot analysis and p53 functionally knock-out cells (A549-E6) were used. Results : SNP and SNAP induced dose-dependent cell death in A549 cells and fluorescent microscopy revealed that SNAP induced apoptosis in low doses but necrosis in high doses while SNP induced exclusively necrotic cell death. Iron inhibition study using RBCs and FeSO4 significantly blocked SNAP-induced cell death. And also SNAP-induced cell death was blocked by bcl-2 overexpression. Finally, we found that SNAP activate p53 by Western blot analysis and that SNAP-induced cell death was decreased in the abscence of p53. Conclusion : In lung epithelial cells, NO can induce cell death, more precisely apoptosis in low doses and necrosis in high doses. And iron, bcl-2, and p53 play important roles in NO-induced cell death.