• Title/Summary/Keyword: SK-N-SH human neuronal cells

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Effects of Cordyceps ophioglossoides extracts on the neuronal death and memory dificits

  • Park, Byung-Chul;Jin, Da-Qing;Beak, Sung-Mok;Lee, Jae-Sung;Choi, Hee-Don;Kim, Jung-Ae
    • Proceedings of the PSK Conference
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    • 2003.10b
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    • pp.124.1-124.1
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    • 2003
  • We investigated whether the mushroom extracts can protect neuronal death and ameliorate memory deficits in Alzheimer"s disease induced by $\beta$-amyloid peptide[A$\beta$(25-35)]. Cellular model of Alzheimer"s disease was produced by using SK-N-SH human neuronal cells treated with $A\beta$. Treatment with 40uM $A\beta$ for 48hours caused a 46% loss of cell viability. First, we examined the effects of 22 mushroom extracts on neuronal death using MTT assay. We found that 3 mushroom extracts increased viability of the cells from 46% to 87%. (omitted)

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Effect of 1,2,3,4,6-penta-O-gallolyl-β-ᴅ-glucose on markers of cognitive function in human neuroblastoma SK-N-SH cell line (1,2,3,4,6-Penta-O-gallolyl-β-ᴅ-glucose가 인간 유래 신경모세포주인 SK-N-SH세포의 인지기능 표지자에 미치는 영향)

  • Yoon, Hyeon Seok;Park, So Yeon;Kim, Yoon Hee
    • Korean Journal of Food Science and Technology
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    • v.53 no.6
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    • pp.715-721
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    • 2021
  • Cognitive impairment and Alzheimer's disease are serious social problems associated with the rising elderly population in Korea. 1,2,3,4,6-Penta-O-galloyl-β-ᴅ-glucopyranose (PGG) is a gallotannin isolated from medicinal plants such as Rhus chinensis. This study was performed to evaluate the effect of PGG on biomarkers related to cognitive function in human neuroblastoma SK-N-SH cells. Inhibition of acetylcholinesterase (AChE) activity is considered to be one of the main therapeutic strategies. PGG inhibited AChE activity in the test tube as well as in SK-N-SH cells. In addition, PGG induced protein and mRNA expression of brain-derived neurotrophic factor (BDNF), which is a mammalian neurotrophin that plays major roles in the development, maintenance, repair, and survival of neuronal populations. As one of the underlying molecular mechanisms that induce BDNF expression, PGG induced the activation of Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII)-cAMP response element binding protein (CREB) pathway. In conclusion, PGG may be an useful material for improving cognitive function.

6-Hydroxydopamine-induced Adaptive Increase in GSH Is Dependent on Reactive Oxygen Species and Ca2+ but not on Extracellular Signal-regulated Kinase in SK-N-SH Human Neuroblastoma Cells

  • JIN Da-Qing;Park Byung CHUL;KIM Jung-Ae
    • Biomolecules & Therapeutics
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    • v.13 no.4
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    • pp.256-262
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    • 2005
  • We examined the signaling molecules involved in the 6-hydroxydopamine (6-OHDA)-induced neuronal cell death and increase in cellular glutathione (GSH) level in SK-N-SH cells. The 6-OH-DA-induced cell death was significantly prevented by the pretreatment with N-acetylcysteine (NAC), a thiol antioxidant, and BAPTA, an intracellular $Ca^{2+}$ chelator. Although 6-OHDA induced ERK phosphorylation, the pretreatment with PD98059, an ERK inhibitor, did not block 6-OHDA-induced cell death. In addition, the 6-OHDA-induced activation of caspase-3, a key signal for apoptosis, was blocked by the pretreatment with NAC and BAPTA. While the level of reactive oxygen species (ROS) was significantly increased in the 6-OHDA-treated cells, the cellular GSH level was not altered for the first 6-hr exposure to 6-OHDA, but after then, the level was significantly increased, which was also blocked by the pretreatment with NAC and BAPTA, but not by PD98059. Depletion of GSH by pretreating the cells with DL-buthionine-(S,R)-sulfoximine (BSO), a glutathione synthesis inhibitor, rather significantly potentiated the 6-OHDA-induced death. In contrast to the pretreatment with NAC, 6-OHDA-induced cell death was not prevented by the post-treatment with NAC 30 min after 6-OHDA treatment. The results indicate that the GSH level which is increased adaptively by the 6-OHDA-induced ROS and intracellular $Ca^{2+}$ is not enough to overcome the death signal mediated through ROS-$Ca^{2+}$ -caspase pathway.

Antioxidant Activity and Inhibitory Effect against Oxidative Neuronal Cell Death of Kimchi Containing a Mixture of Wild Vegetables with Nitrite Scavenging Activity (아질산염 소거 작용을 가진 산채 혼합물을 함유한 김치의 항산화 활성 및 산화적 신경세포 사멸 억제 효과)

  • Kang, Kyung Hun;Park, Si Young;Kwon, Ki Han;Lim, Heekyung;Kim, Sung Hyun;Kim, Jeong Gyun;Chung, Mi Ja
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.44 no.10
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    • pp.1458-1469
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    • 2015
  • This study was carried out to investigate the nitrite scavenging activities (NSA) of nine kinds of wild vegetables in a $NaNO_2$ model system and nitrite of Chinese cabbage as well as the inhibitory effect of kimchi containing a mixture of wild vegetables (MWV) with nitrite scavenging activity on brain neuronal cell death. NSA was higher at pH 1.2 than pH 4.2 in all samples. NSA of extracts from sprouts of Oenothera laciniata and Aster scaber (AS) was above 90% at pH 1.2. AS, Codonopsis lanceolate (CL), Adenophora triphylla (AT), Platycodon grandiflorum (PG), and Taraxacum officinale (TO) extracts showed significantly higher levels of NSA than those from other extracts at pH 4.2. CL, AT, PG, and TO extracts showed high NSA on nitrite of Chinese cabbage. In addition, the effects of MWV on antioxidant and brain neuronal cell death induced by oxidative stress were investigated in human brain neuroblastoma SK-N-SH cells. MWV extract attenuated $H_2O_2$-induced cell death and reactive oxygen species (ROS) generation in SK-N-SH cells. MWV extract showed significantly higher DPPH radical scavenger activity when compared to normal kimchi extract. MWV extract showed an inhibitory effect on brain neuronal cell death against oxidative stress by antioxidant activities.