• Korean Journal of Food Science and Technology
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• v.46 no.5
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• pp.609-615
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• 2014

The cytoprotective effect of Moringa oleifera Lam. (drumstick tree) on neuronal cells was investigated to confirm the physiological benefits associated with this natural food resource. First, the drumstick tree extract was chemically analyzed to determine inherent nutritional constituents. Calcium and potassium were identified as the major mineral constituents, and palmitic acid (C16:0, 16.33%) and gadoleic acid (C20:01, 66.34%) were detected as the major fatty acids. Moreover, drumstick tree extract contained 94.78 mg/100 g vitamin E and 112.61 mg/100 g niacin. PC12 cells were used to study the cytoprotective effects of drumstick tree extract. Intracellular accumulation of reactive oxygen species was significantly reduced when $H_2O_2$ treated-neuronal cells were cultured in a medium containing the methanolic extract of drumstick tree, compared to cells treated with only $H_2O_2$. Cell viability assay using MTT showed that the extract protected cells against $H_2O_2$-induced neurotoxicity and inhibited LDH leakage from the cell membrane. Caspase assay showed that the extract exerted cytoprotective effect against apoptosis. Consequently, these data suggest that drumstick tree is a useful natural resource with positive effects on human health.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.2
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• pp.507-516
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• 2004

Alzheimer's disease(AD) is a geriatric dementia that is widespread in old age. In the near future AD will be the commom disease in public health service. Although a variety of oriental presciptions in study POD(Polygala tenuifolia extracted from dichlorometan) have been traditionally utilized for the treatment of AD, their pharmacological effects and action mechanisms have not yet fully elucidated. It has been widely believed that AP peptide divided from APP causes apoptotic neurotoxicity in AD brain. However, recent evidence suggests that CT105, carboxy terminal 105 aminoacids peptide fragment of APP, may be an important factor causing neurotoxicity in AD. SK-N-SH cells expressed with CT105 exhibited remarkable apoptotic cell damage. Based on morphological observations by phase contrast microscope and NO formation in the culture media, the CT105-induced cell death was significantly inhibited by POD. In addition, AD is one of brain degeneration disease. So We studied on herbal medicine that have a relation of brain degeneration. From old times, In Oriental Medicine, PO water extract has been used for disease in relation to brain degeneration. We were examined by ROS formation, neurite outgrowth assay and DPPH scravage assay. Additionally, we investigated the association between the CT105 and neurite degeneration caused by CT105-induced apoptotic response in neurone cells. We studied on the regeneratory and inhibitory effects of anti-Alzheimer disease in pCT105-induced neuroblastoma cell lines by POD. Findings from our experiments have shown that POD inhibits the synthesis or activities of CT105, which has neurotoxityies and apoptotic activities in cell line. In addition, treatment of POD(>50 ㎍/㎖ for 12 hours) partially prevented CT(105)-induced cytotoxicity in SK-N-SH cell lines, and were inhibited by the treatment with its. POD(>50 ㎍/㎖ for 12 hours) repaired CT105-induced neurite outgrowth when SK-N-SH cell lines was transfected with CT105. As the result of this study, In POD group, the apoptosis in the nervous system is inhibited, the repair against the degerneration of Neuroblastoma cells by CT105 expression is promoted. Decrease of memory induced by injection of scopolamin into rat was also attenuted by POD, based on passive avoidance test. Taken together, POD exhibited inhibition of CT105-induced apoptotic cell death. POD was found to reduce the activity of AchE and induced about the CA1 in rat hippocampus. Base on these findings, POD may be beneficial for the treatment of AD.

• The Journal of Korean Medicine
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• v.27 no.2 s.66
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• pp.122-133
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• 2006

Objectives : The amyloid $\beta$-protein ($A\beta$) is the principal component of the senile plaques characteristic of Alzheimer's disease (AD) and elicits a toxic effect on neurons in vitro and in vivo. Many environmental factors including antioxidants and proteoglycans modify $A{\beta}toxicity$. In this study, we have investigated the protective effects of water- and organic solvent-extracts of Hemerocallis fulva root fractions pre-extracted with methanol on $A\beta$-induced oxidative cell death in cultured rat pheochromocytoma (PC12) cells. Methods : For this study, we used MTT reduction assay for detection of protective effects of water- and organic solvent-extracts of Hemerocallis fulva root fractions pre-extracted with methanol on $A{\beta}_{25-35}$-induced cytotoxicity to PC12 cells. We also used cell-based $\beta$-secretase assay system to investigate the inhibitory effect of water- and organic solvent-extracts of Hemerocallis fulva root on $\beta$-secretase activity. Results : We previously reported that methanol extracts of Hemerocallis fulva root strongly attenuated cytotoxicity induced by the three $A\beta$ fragments ($A{\beta}_{25-35},\;A{\beta}_{1-42}\;A{\beta}_{1-43}$) to both SK-N-MC and PC12 cells. In the present study, we found that butanol-, ethylacetate-, chloroform-, and water-extracts of Hemerocallis fulva root fractions pre-extracted with methanol had strong protective effects against $A{\beta}_{25-35}$-induced cytotoxicity to PC12 cells and inhibitory potency to $\beta$-secretase activity. Conclusion : These results suggest that butanol-, ethylacetate-, chloroform-, and water-extracts of Hemerocallis fulva root fractions pre-extracted with methanol may contain the protective component(s) against $A\beta$-induced cell death in PC12 cells as well as inhibitory component(s) to $\beta$-secretase activity.

• Journal of the Korean Applied Science and Technology
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• v.37 no.4
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• pp.744-754
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• 2020

We investigated the whether endurance exercise and MitoQ intake mediated neuroprotection are associated with mitochondrial function in 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine(MPTP) -induced mice model of Parkinson's disease. C57BL/6 male mice were randomly assigned to five groups: Normal Conrol(NC, n=10), MPTP Control(MC, n=10), MPTP +MitoQ(MQ, n=10), MPTP + Exercise(ME, n=10) and MPTP + MitoQ + Exercise(MQE, n=10). Exercise intervention groups performed the treadmill exercise for 5days/week for 5 weeks with gradual increase of intensity. MitoQ intake groups consumed the MitoQ at a concentration of 250μmol by dissolving with water during experiment period. Our data demonstrated that ME and MQE group restored MPTP-induced motor dysfunction. In addition, treatment groups(MQ, ME and MQE) increased tyrosine hydroxylase levels, and suppressed the accumulation of α-synuclein levels. Futhermore, treatment groups modulated the mitochondrial function such as upregulated mitochondrial biogenesis, increased antioxidant enzyme, enhanced a anti-apoptotic protein(e.g., BCL2), and reduced a pro-apoptotic protein(e.g., BAX). Taken together, these results suggested that endurance exercise and MitoQ intake-mediated increase in mitochondrial function contributes to improvement of aggravated dopaminergic neuronal, resulting in attenuation of motor function of Parkinson's disease.

• International Journal of Oral Biology
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• v.32 no.2
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• pp.51-57
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• 2007

Cyclosporin A (CsA) plays an important role in clinical medicine and basic biology as an immunosuppressant and a mitochondrial permeability blocker, respectively. It was reported that CsA has a protective role by preventing apoptosis and promoting the proliferation in severed neurons. However, the molecular mechanisms for CsA-induced neuronal cell proliferation are unclear. In this study, we examined the mechanisms underlying the CsA-induced proliferation of PC12 cells. CsA increased the viability of PC12 cells in a dose(over $0.1{\sim}10\;{\mu}M$)-and time-dependent manner. The level of ROS generation was decreased in the CsA-treated PC12 cells. Expression of Bcl-2, an antiapoptotic molecule that inhibits the release of cytochrome c from the mitochondria into the cytosol, was upregulated, whereas Bax, a proapototic molecule, was not changed in the CsA-treated PC12 cells. CsA downregulated the mRNA expression of VDAC 1 and VDAC 3, but VDAC 2 was not changed in the CsA-treated PC12 cells. The level of cytosolic cytochrome c released from the mitochondria and the caspase-3 activity were attenuated in the CsA-treated PC12 cells. These results suggest that the mitochondria-mediated apoptotic signal and Bcl-2 family may play an important role in CsA-induced proliferation in PC12 cells.

• The Journal of Korean Medicine
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• v.28 no.2 s.70
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• pp.213-223
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• 2007

Objective : Alzheimer's disease (AD) is a geriatric dementia that is widespread in old age. With an aging populace, AD is a looming problem in public health service. Alzheimer's disease is characterized by specific neuronal degeneration in certain areas of the brain. Mutations and abnormal expression of several genes are associated with ${\beta}-amyloid$ deposits and Alzheimer's disease; among them APP, PS1, and PS2, SOD, free radical, ROS. Methods:We studied herbal medicines that have a relationship to brain degeneration. From pre-modern times, although a variety of oriental prescriptions of Aster tataricus have been traditionally utilized for the treatment of AD, their pharmacological effects and action mechanisms have not yet been fully elucidated. Result : Based on morphological observations by phase-contrast microscope, TUNEL assay and MTT in the culture media, $H_20_2-induced$ cell death was significantly inhibited by Aticus. We examined by ROS formation, catalase activity and GSH activity. We studied the protective effect and inhibitory effects of neurotoxicity in $H_20_2-induced$ PC-12 cells by Aticus. Findings from our experiments show that Aticus inhibits apoptosis, which has neurotoxicities and cell damage in PC-12 cells. In addition, treatment with Aticus ($>25{\mu}g/ml$ for 6hrs) partially prevented $H_20_2-induced$ cytotoxicity in PC-12 cells, and induced a protective effect. Conclusion : As the result of this study, in the Aticus group, the apoptosis in the nervous system was inhibited, protected against the degeneration of PC-12 cells by $H_20_2$. Taken together, Aticus exhibited inhibition of $H_20_2-induced$ apoptotic cell death. Aticus was found to induce protective effect on GSH and catalase in PC-12 cells. Based on these findings, Aticus may be beneficial for the treatment of AD.

• KOREAN JOURNAL OF CROP SCIENCE
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• v.55 no.1
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• pp.65-69
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• 2010

This study was carried out to investigate the antioxidative and anti-inflammatory activity of crude anthocyanin compounds extracted from black soybean. The crude anthocyanin compounds were extracted with 80% methanol and concentrated to powder. The most abundant compound isolated from the extract was C3G(cyanidin-3-glucoside). The superoxide dismutase (SOD) assay was conducted to assess the antioxidative activity of the crude extract. SOD, which catalyzes the dismutation of the superoxide anion into hydrogen peroxide and molecular oxygen, is one of the most important antioxidative enzymes. The black soybean anthocyanin extracts inhibited more than 90% of the superoxide radical at a concentration of 0.1% and 100% at a concentration of 0.5%, indicating that this extract displayed excellent antioxidative activity. To assess the anti-inflammatory activity of the extract, a NO(Nitric oxide) production assay in RAW 264.7 cells was performed. NO is an important physiological messenger and effector molecule in many biological systems, including immunological, neuronal and cardiovascular tissues. In this assay, the anthocyanin extracts showed a high anti-inflammatory potential, where the inhibitory potency for NO production was similar to the positive control, particularly for EGCG(epigallocatechin-3-gallate), which is known to have excellent anti-inflammatory activity. Thus, it can be concluded that the anthocyanin extracts from black soybean have distinctive pharmaceutical activities and may be used as an excellent source materials to supplement the health benefits of various food products.

• Applied Microscopy
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• v.41 no.4
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• pp.249-255
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• 2011

Neurons utilize a large quantity of energy for their survival and function, and thereby require active mitochondrial function. Mitochondrial morphology shows dynamic changes, depending on the cellular condition, and mitochondrial dynamics are required for neuronal development and function. In this study, we found that the length of mitochondria in the distal axon is significantly shorter than that of mitochondria in dendrites or proximal axons of cerebral cortical neurons, and the reason for this difference is the local fission within the axon. We also found that suppression of Drp1, a key regulator of mitochondrial fission, resulted in significant elongation of mitochondria in axons. Collectively, these results suggest that local mitochondrial fission within the axon contributes to region-dependent mitochondrial length differences in the axons of cortical neurons.

• Journal of Life Science
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• v.28 no.11
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• pp.1386-1395
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• 2018

Over recent years, it has become evident that the central nervous system bidirectionally interacts with the gastrointestinal tract along the gut-brain axis. A series of preclinical studies indicate that the gut microbiota can modulate central nervous system function through a multitude of physiological functions. Polyphenols are ubiquitous plant chemicals included in foods such as fruits, vegetables, tea, coffee and wine, and their consumption is directly responsible for beneficial health effects due to antioxidant, anti-inflammatory, antimicrobial, immunomodulatory, anticancer, vasodilating, and prebiotic-like effects. There is increasing evidence that dietary polyphenol can contribute to beneficial effects in neuronal protection acting against oxidative stress and inflammatory injury as well as in cognitive functions. In this paper, we overview the neuroprotective role of dietary polyphenols especially focusing on the neuroinflammation and neurovascular function by interaction with the gut microbiome. Polyphenol metabolites could directly act as neurotransmitters crossing the blood-brain barrier and modulating the cerebrovascular system or indirectly modulating gut microbiota. In addition, evidence suggests that dietary polyphenols are effective in preventing and managing neurological disorders, such as age-related cognitive decline and neurodegeneration, through a multitude of physiological functions. Dietary polyphenols are increasingly envisaged as a potential nutraceuticals in the prevention and treatment of neurological disorders, because they possess the ability to reduce neuroinflammation, to improve memory and cognitive function and to modulate the gut microbiota.

• Korean Journal of Clinical Laboratory Science
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• v.52 no.4
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• pp.408-416
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• 2020

This study examined the neuronal cytotoxicity of aluminum chloride (AlCl3), a dementia inducer, and the protective effects of Aster yomena (Kitam.)(AY) extract on AlCl3-induced cytotoxicity in cultured C6 glioma cells. The antioxidative effects, such as the inhibitory ability of xanthine oxidase (XO) and superoxide anion-radical (SAR) scavenging ability, on cell viability were examined. AlCl3 decreased the cell viability significantly in a dose-dependent manner, and the XTT50 value was 130.0 μM in these cultures. The cytotoxicity of AlCl3 was determined to be mid-toxic according to the Borenfreund and Puerner' toxic criteria. Quercetin (QU), an antioxidant, increased the cell viability reduced by AlCl3-induced cytotoxicity. The protective effect of the AY extract on AlCl3-induced cytotoxicity was analyzed. The AY extract increased the cell viability remarkably compared to the AlCl3-treated group and showed the inhibitory ability of XO and SAR-scavenging ability. The cytotoxicity of AlCl3 was correlated with oxidative stress, and the AY extract effectively prevented AlCl3-induced cytotoxicity through its antioxidative effects. In conclusion, natural resources, such as the AY extract, may be a putative agent for improving the cytotoxicity of heavy metallic compounds correlated with oxidative stress, such as AlCl3, a morbid agent.