• 대한본초학회지
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• 제27권6호
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• pp.83-90
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• 2012

Objectives : Modified Bo-Yang-Hwan-O-Tang (mBHT) is a polyherbal medicine of twelve herbs traditionally used in the treatment of cerebral and cardiac stroke and vascular dementia. The purpose of this study was to evaluate the neuroprotective effect, pyramidal neuronal cell, inflammation and apoptosis of mBHT against global ischemia in rats. Methods : Global ischemia was produced by two-vessel occlusion(2-VO) in SD male rats. mBHT at dose of 500 mg/kg was orally administrated for 2 weeks or 6 weeks after global ischemia. The histopathological changes of ischemic brain were observed by staining of hematoxylin and eosin (H&E) and Nissl and immunohistochemisty with anti-GFAP (glial fibrillary acidic protein) antibody as a astrocyte marker. The expression of inducible nitric oxide synthase (iNOS) and apoptotic proteins such as Bax, Bcl-2 and caspase-3 was determined by western blot. Results : mBHT treatment significantly inhibited the pyramidal neuronal loss in CA1 of hippocampus of global ischemic rats by 2-VO. mBHT also suppressed the activation of astrocytes in the CA1 at 6 weeks after ischemia. In addition, mBHT significantly increased the expression of anti-apoptotic protein, Bcl-2 on iscemic brain, and significantly attenuated the expression of apoptotic proteins, Bax and caspase-3. Conclusions : These results indicate that mBHT inhibits neuronal cell damage induced in global ischemia by 2-VO, suggesting that mBHT may be a potential candidate for the treatment of vascular dementia.

• The Korean Journal of Physiology and Pharmacology
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• 제15권6호
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• pp.353-361
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• 2011

In this study, cyanidin-3-glucoside (C3G) fraction extracted from the mulberry fruit (Morus alba L.) was investigated for its neuroprotective effects against oxygen-glucose deprivation (OGD) and glutamate-induced cell death in rat primary cortical neurons. Cell membrane damage and mitochondrial function were assessed by LDH release and MTT reduction assays, respectively. A time-course study of OGD-induced cell death of primary cortical neurons at 7 days in vitro (DIV) indicated that neuronal death was OGD duration-dependent. It was also demonstrated that OGD for 3.5 h resulted in approximately 50% cell death, as determined by the LDH release assay. Treatments with mulberry C3G fraction prevented membrane damage and preserved the mitochondrial function of the primary cortical neurons exposed to OGD for 3.5 h in a concentration-dependent manner. Glutamate-induced cell death was more pronounced in DIV-9 and DIV-11 cells than that in DIV-7 neurons, and an application of $50{\mu}M$ glutamate was shown to induce approximately 40% cell death in DIV-9 neurons. Interestingly, treatment with mulberry C3G fraction did not provide a protective effect against glutamate-induced cell death in primary cortical neurons. On the other hand, treatment with mulberry C3G fraction maintained the mitochondrial membrane potential (MMP) in primary cortical neurons exposed to OGD as assessed by the intensity of rhodamine-123 fluorescence. These results therefore suggest that the neuroprotective effects of mulberry C3G fraction are mediated by the maintenance of the MMP and mitochondrial function but not by attenuating glutamate-induced excitotoxicity in rat primary cortical neurons.

• Food Science and Biotechnology
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• 제16권5호
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• pp.858-862
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• 2007

The present study was conducted to examine the antioxidant activities and neuroprotective effects of methanolic extracts from Schizonepeta tenuifolia Briquet (STE). STE ($100\;{\mu}g/mL$) showed $43.33\;{\mu}M$ of total phenolic content, 64.43% of radical scavenging activity, and 0.157 of reducing power. In addition, the effect of STE on $H_2O_2$-induced DNA damage in human leucocytes was evaluated by the comet assay, where STE was a dose dependent inhibitor of DNA damage induced by $200{\mu}M$ of $H_2O_2$. The protective effect of STE against $H_2O_2$-induced oxidative damage on PC12 cells was investigated by an 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) reduction assay and lactate dehydrogenase (LDH) release assays. After 2 hr of cell exposure to $H_2O_2\;(500\;{\mu}M)$, a marked reduction in cell survival was observed. However, this reduction was significantly prevented by $1-50\;{\mu}g/mL$ of STE. Therefore, these results suggest that STE could be a new antioxidant candidate against neuronal diseases.

• 동의생리병리학회지
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• 제33권1호
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• pp.10-16
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• 2019

In order to investigate the effects of Eucomiae Cortex extracts on the depression caused by aging, histochemistry and immunohistochemistry were performed on the hippocampus of aged rats and the following results were obtained. Experimental animals were divided into three groups as follows: 8 week old ICR male mice, Aging-elicited group (AE group) and Eucomiae Cortex treatment group (EC group) 50 week old male ICR mice were used. The control group and AE group did not take any treatment and did not restrict diets and negatives. In the EC group, 0.51g/kg of Eucomiae Cortex extract was dissolved in distilled water once a day for 6 months. The Eucomiae Cortex extract reduced pyramidal neuronal damage in C3 hippocampus and dentate gyrus, increased DJ-1, SHH positive responses in aged mouse hippocampus, and 8-OHdG positivity was reduced, ${\beta}$-endorphin positivity was reduced in aged mouse substantia nigra. Therefore, based on the above results, Eucomiae Cortex extract reduces damage of pyramidal neurons in the hippocampus caused by aging, inhibits neuronal cell death, induces proliferation and differentiation of stem cells in the hippocampus, reduces DNA damage-induced oxidative stress, so improves the reduction of hippocampus volume. It is also thought to improves depression due to aging through ${\beta}$-endorphin which enhances mood through the inhibition of pain.

• 동의생리병리학회지
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• 제18권2호
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• pp.490-495
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• 2004

Brain cells produce cytokines and chemokines during the inflammatory process of many neuronal diseases both in animal models and in patients. Inflammatory cytokines are the main responsible for the onset of inflammatory cascade. During the past decade, a growing corpus of evidence has indicated an important role of these cytokines in the development of brain damage. ZhenganXifeng-tang (ZGXFT) is a Korean herbal prescription, which has been successfully applied for the treatment of various neuronal diseases. However, its effect in experimental models remains unknown. Astrocytes are predominant neuroglial cells of the central nervous system and are actively involved in cytokine-mediated events in inflammatory disease. An inflammatory response associated with β-amyloid (Aβ) and interleukin (IL)-1β is responsible for the pathology of inflammation disease. To investigate the biological effect of ZGXFT, the author examined cytotoxicity, effect of cytokines (IL-6 and IL-8) secretion and expression of cyclooxygenase-2 (COX-2) on human astrocytoma cell line U373MG stimulated with IL-1β plus M fragment 25-35 (Aβ [25-35]). ZGXFT by itself had no effect on cell viability on human astrocytoma cells. The secretion of IL-6 and IL-8 was inhibited by pre-treatment with ZGXFT in human astrocytoma cells. In addition, the expression of COX-2 was induced by IL-1β plus AB[25-35] and was partially inhibited by treatment with ZGXFT. The author demonstrates the regulatory effects of inflammatory reactions by ZGXFT in human astrocytes for the first time and suggest the anti-inflammatory effect of ZGXFT may reduce and delay pathologic events of inflammatory disease.

• 동의생리병리학회지
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• 제24권3호
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• pp.401-409
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• 2010

This study was designed to investigate the effects of BojungIkkiTang-Gamybang freeze dried powder (BITG) on proliferauion, protective of cell death induced by chemicals such as paraquat, hydrogen peroxide etc and anti-oxidative effects in C6 glioma cells. In our results, BITC accelerated proliferation rates of C6 cells in vitro. In addition, protective effects on cell death induced by paraquat and hydrogen peroxide. And, BITC did not have effects on SOD and total glutathione activities, but decresed malone dialdehyde activity. In conclusion, these results suggest the possibility of BojungIkkiTang-Gamybang to protect brain cell or neuronal cell from damage induced by oxidative stress. And also suggest that related mechanisms are involved in malone dialdehyde activity.

• 대한한의학회지
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• 제29권2호
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• pp.151-164
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• 2008

Objective: To investigate the effects of Yeongdamsagantang (YDGT) on apoptosis of neuronal cells that can result in dementia. Method: The water extract of the YDGT was tested in vitro for its beneficial effects on neuronal survival and neuroprotective functions, particularly in connection with $A{\beta}$ oligomer-related dementias. $A{\beta}$ oligomers derived from proteolytic processing of the ${\beta}-amyloid$ precursor protein (APP), including the $amyloid-{\beta}$ peptide $(A{\beta})$, play a critical role in the pathogenesis of Alzheimer's disease. A neuroblastoma cell line stably expressing an $A{\beta}$ oligomerassociated neuronal degeneration was used to investigate if YDGT inhibits formation of $A{\beta}$ oligomer. To measure the ATP generating level in mitochondrial membrane, luciferin/luciferase luminescence kit (Promega) and luminator was used, and to survey the protein's apparition, confocal microscopy was used. Result: $A{\beta}oligomer$ had a profound attenuation in the increase in CT105 expressing neuro2A cells from YDGT. Experimental evidence indicates that YDGT protected against neuronal damage from cells, but its cellular and molecular mechanisms remain unknown. We demonstrated that YDGT inhibited formation of $amyloid-{\beta}$ $(A{\beta})$ oligomers, which were the behavior, and possibly causative, features of AD. The decreased $A{\beta}$ oligomer in the presence of YDGT was observed in the conditioned medium of this $A{\beta}oligomer-secreting$ cell line under in vitro. In the cells, YDGT significantly attenuated mitochondrion-initiated apoptosis. Conclusion: (i) a direct $A{\beta}$ oligomer toxicity and the apoptosis initiated by the mitochondria; and (ii) multiple cellular and molecular neuroprotective mechanisms, including attenuation of apoptosis and direct inhibition of $A{\beta}$ oligomer aggregation, underlie the neuroprotective effects of YDGT.

• 한국잠사학회:학술대회논문집
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• 한국잠사학회 2003년도 International Symposium of Silkworm/Insect Biotechnology and Annual Meeting of Korea Society of Sericultural Science
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• pp.112-113
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• 2003

Kynurenic acid (KYNA), tryptophan metabolite is known to have cell protective effect against various insults in the brain. But so far, the protective mechanism is largely unknown. In this study, we investigated how the KYNA exerts protective effect against 6-OHDA, a causative molecule of Parkinsonian syndrome, using SH-SY5Y cells. (omitted)

• 대한방사성의약품학회지
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• 제6권2호
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• pp.116-130
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• 2020

The aging society is globally one of biggest issue because it is related with various degenerative brain disease such as dementia, Parkinson's disease, Alzheimer's disease, multiple sclerosis, and cerebrovascular disease. These diseases are characterized by misfolded-protein aggregation; another pathological trait is "neuroinflammation". In physiological state, the resting microglia cells are activated and it removes abnormal synapses and cell membrane debris to maintain the homeostasis. In pathological state, however, microglia undergo morphological change form 'resting' to 'activated amoeboid phenotype' and the microglia cells are accumulated by neuronal damage, the inflammatory reactions induced nerve metamorphosis with a variety of neurotoxic factors including cytokines, chemokines, and reactive oxygen species. Thus, the activated microglia cell with various receptors (TSPO, COX, CR, P2XR, etc.) was perceived as important biomarkers for imaging the inflammatory progression. In this review, we would like to introduce the current status of the development of radiotracers that can image activated microglia.

• 한국식품과학회지
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• 제41권1호
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• pp.87-92
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• 2009

본 연구에서는 금불초(Inula britannica) 추출물의 항산화 효과와 ${H_2}{O_2}$로부터 유도된 SH-SY5Y 신경모세포종의 세포독성에 대한 보호능을 측정하였다. 금불초 지상부위의 70% 메탄올 추출물에 대하여 용매별로 분획을 실시하였고 핵산(Fr.H), 에틸아세테이트(Fr.EA) 및 물(Fr.W) 분획에 대하여 활성을 조사하였다. 분획 중 Fr.W의 폴리페놀/플라보노이드 함량이 가장 높았으며 Fr.W의 총 폴리페놀 함량은 $318.1{\pm}20.6{\mu}g$/mg solid로, Fr.EA 및 Fr.H와 비교하여 각각 약 2.5배, 23.1배 수준이었다. DPPH radical, ABTS radical 및 nitric oxide 소거능 등의 항산화 활성에서도 Fr.W가 가장 높은 활성을 나타내었고 Fr.H는 거의 활성을 나타내지 않았다. Fr.W는 ${H_2}{O_2}$에 의해 유도된 세포사멸에 대하여 62.5 ${\mu}g$/mL 농도에서 현저하게 세포독성을 감소시켰으며 250 ${\mu}g$/mL에서는 77.0%의 세포사멸 억제능을 보였다. Fr.EA는 보호 효과를 나타 내지 않았으며 Fr.H는 오히려 ${H_2}{O_2}$로 인한 세포 독성을 증가시키는 것으로 나타났다. 세포 내 ROS에 대한 영향으로 Fr.W 250 ${\mu}g$/mL 처리시 39.2% 세포내 ROS를 감소시켰으며 Fr.EA는 25 ${\mu}g$/mL에서 26.8%의 세포내 ROS를 소거하였다. 이러한 금불초 Fr.W의 항산화 활성은 ROS에 의해 야기되는 뇌세포 독성에 대한 보호 작용에 공헌할 수 있을 것으로 예상된다.