• 한국수산과학회지
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• 제52권1호
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• pp.81-86
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• 2019

The common hallmark of several neurodegenerative disorders, including Alzheimer's disease (AD), is the presence of chronic neuroinflammation, which contributes to the loss of neuronal structure and function. This study investigated the effects of an ethanolic extract of Sargassum serratifolium (SSE) in a lipopolysaccharides (LPS)-induced murine neuroinflammation model. Mice were administered SSE (100 mg/kg body weight) or vehicle for 5 days by oral gavage, and then treated with LPS or saline by intraperitoneal injection. Thereafter, the brain tissues were collected, and the expression of pro-inflammatory cytokines was analyzed by quantitative real-time RT-PCR. There was a marked increase in the spleen weight index in the LPS-treated groups, which indicated the induction of acute systemic inflammation. Based on significant increases in the levels of IL-1 and IL-6 expression, the induction of neuroinflammation was also evident in the cortex and hippocampus of the LPS-treated groups. The overall expression of IL-1 and IL-6 was decreased slightly by SSE administration, compared with the LPS group, and a marked change in IL-1 was observed in the cortex of the SSE-treated (SSE/LPS) group. These results suggest that SSE has potential as an anti-neuroinflammatory nutraceutical.

• 대한본초학회지
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• 제28권2호
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• pp.93-101
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• 2013

Objects : Baicalein is a major bioactive flavonoid component of Scutellaria baicalensis Georgi that shows a wide range of biological activities, including neuroprotections and anti-inflammatory actions. Hence it is a potential therapeutic material for the treatment of neuroinflammation. In this study, we investigated the modulatory effect of baicalein on neuroinflammation. Method : Pro-inflammatory cytokines (TNF-${\alpha}$, IL-$1{\beta}$ and IL-6 mRNA), COX-2 mRNA expression and microglial activation in the brain tissue is induced by systemic lipopolysaccharide (LPS) treatment in C57BL/6 mice. Baicalein was treated orally with 10, 20, and 30 mg/kg 1 hour prior to the LPS (3 mg/kg, i.p.) injection. TNF-${\alpha}$, IL-$1{\beta}$, IL-6 and COX-2 mRNA expression in the brain tissue was measured by the quantitative real-time polymerase chain reaction(PCR) method. Iba1 expression in the brain was measured by western blotting method. Microglia was observed with immunohistochemistry. Results : Baicalein 30 mg/kg significantly attenuated the expression of TNF-${\alpha}$, IL-$1{\beta}$, IL-6 and COX-2 mRNA in the brain tissue. Baicalein 20 mg/kg significantly attenuated the expression of IL-6 mRNA in the brain tissue. Baicalein 30 mg/kg significantly attenuated the expression of Iba1 protein expression in the brain tissue. Baicalein 30 mg/kg significantly decreased the number and cell size of microglia in the cerebral cortex and hypothalamic region and the area percentage of Iba1-expressed microglia in the hippocampus. Conclusion : These results demonstrated that baicalein attenuates LPS induced neuroinflammation in the mice via reduction of pro-inflammatory cytokines (TNF-${\alpha}$, IL-$1{\beta}$, IL-6), COX-2 mRNA expression and microglial activation.

• BMB Reports
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• 제53권1호
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• pp.28-34
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• 2020

Sphingolipids are ubiquitous building blocks of eukaryotic cell membranes that function as signaling molecules for regulating a diverse range of cellular processes, including cell proliferation, growth, survival, immune-cell trafficking, vascular and epithelial integrity, and inflammation. Recently, several studies have highlighted the pivotal role of sphingolipids in neuroinflammatory regulation. Sphingolipids have multiple functions, including induction of the expression of various inflammatory mediators and regulation of neuroinflammation by directly effecting the cells of the central nervous system. Accumulating evidence points to sphingolipid engagement in neuroinflammatory disorders, including Alzheimer's and Parkinson's diseases. Abnormal sphingolipid alterations, which involves an increase in ceramide and a decrease in sphingosine kinase, are observed during neuroinflammatory disease. These trends are observed early during disease development, and thus highlight the potential of sphingolipids as a new therapeutic and diagnostic target for neuroinflammatory diseases.

• Biomolecules & Therapeutics
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• 제19권4호
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• pp.425-430
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• 2011

In this study, we found that Forsythiae fructus (FF) and one of its main compounds, arctigenin, significantly inhibited nitric oxide production in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. Arctigenin also suppressed the expression of inducible nitric oxide synthase and cyclooxygenase-2, and inhibited the activation of extracellular signal-regulated kinase, c-Jun N-terminal kinase and p38. Moreover, it also reduced levels of proinflammatory cytokines, interleukin $1{\beta}$, tumor necrosis factor ${\alpha}$ and prostaglandin E2, and inhibited neuronal death in LPS-treated organotypic hippocampal cultures. Therefore, we suggest that arctigenin may confer a neuroprotective effect via the inhibition of neuroinflammation.

• Biomolecules & Therapeutics
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• 제28권5호
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• pp.381-388
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• 2020

Methamphetamine (METH) is a highly addictive psychostimulant and one of the most widely abused drugs worldwide. The continuous use of METH eventually leads to drug addiction and causes serious health complications, including attention deficit, memory loss and cognitive decline. These neurological complications are strongly associated with METH-induced neurotoxicity and neuroinflammation, which leads to neuronal cell death. The current review investigates the molecular mechanisms underlying METH-mediated neuronal damages. Our analysis demonstrates that the process of neuronal impairment by METH is closely related to oxidative stress, transcription factor activation, DNA damage, excitatory toxicity and various apoptosis pathways. Thus, we reach the conclusion here that METH-induced neuronal damages are attributed to the neurotoxic and neuroinflammatory effect of the drug. This review provides an insight into the mechanisms of METH addiction and contributes to the discovery of therapeutic targets on neurological impairment by METH abuse.

• 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.

• Journal of Nutrition and Health
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• 제50권1호
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• pp.25-31
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• 2017

퇴행성 뇌신경 질환의 원인이 되는 것으로 알려진 미세아교세포의 과도한 활성화에 의한 신경염증반응에 미치는 미역쇠의 보호 효과를 알아보기 위해 LPS를 처리한 BV2 세포에서 미역쇠에서 얻은 에탄올 추출물을 이용하여 실험을 수행하였다. 미세아교세포의 활성화를 유도하는 LPS의 처리는 신경염증반응의 지표인 NO의 생성량과 이들을 조절하는 iNOS, COX-2의 발현을 증가시켰다. 미역쇠 추출물의 처리는 LPS가 유도하는 NO의 생성량을 농도 의존적으로 억제하였고 iNOS와 COX-2의 발현을 억제하여 NO 생성량 저해와 유사한 양상의 결과를 나타내었다. 미역쇠 추출물의 신경 염증반응 저해 효과가 $NF-{\kappa}B$의 활성화 조절을 통해 일어나는지를 알아보기 위해 $NF-{\kappa}B$의 핵으로의 전이, $I{\kappa}B$의 인산화, $NF-{\kappa}B$ 억제제인 PDTC를 이용한 NO의 생성량에 미치는 효과를 확인하였다. 미역쇠 추출물 처리에 의해 핵분획물에서의 $NF-{\kappa}B$ 발현은 현저히 감소하였고 $I{\kappa}B$의 인산화를 억제하였으며 PDTC의 처리로 NO의 생성량은 감소하였다. 이상의 결과는 미세아교세포의 활성화로 인해 발생되는 신경염증반응에 미역쇠 추출물이 $NF-{\kappa}B$의 활성 억제를 통해 NO의 생성을 저해함으로써 항신경염증 효과가 있음을 보여주는 것으로 미역쇠 추출물이 신경염증 관련 뇌신경 질환의 제어하는데 있어서 치료효과를 가지는 소재로서 이용 가능성에 대한 정보를 제공할 것으로 사료된다.

• Bulletin of the Korean Chemical Society
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• 제32권10호
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• pp.3805-3808
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• 2011

• 생약학회지
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• 제45권1호
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• pp.17-22
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• 2014

Grapes has long been used for food, and reported as containing polyphenol which has antioxidant and anti-cancer effects. Neuroinflammation is chronic inflammation at the brain, lead to neurodegenerative diseases. In this study, quercetin-3-O-glucuronide (QG) isolated from the leaf of Vitis labruscana has anti-neuroinflammatory effects. QG were investigated using MTT assay, western blot, nitric oxide (NO) assay, prostaglandin $E_2$ ($PGE_2$) assay, cytokine assay in lipopolysaccharide (LPS)-induced inflammation in BV2 cells. QG dose-dependently attenuated the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), accordingly inhibited the production of NO and $PGE_2$. QG decreases the levels of proinflammatory cytokine such as tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interlukin-$1{\beta}$ (IL-$1{\beta}$). Thereby, QG may offer therapeutic potential for treatment of neurodegenerative disease related to neuroinflammation.

• The Korean Journal of Physiology and Pharmacology
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• 제22권3호
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• pp.301-309
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• 2018

Statins mediate vascular protection and reduce the prevalence of cardiovascular diseases. Recent work indicates that statins have anticonvulsive effects in the brain; however, little is known about the precise mechanism for its protective effect in kainic acid (KA)-induced seizures. Here, we investigated the protective effects of atorvastatin pretreatment on KA-induced neuroinflammation and hippocampal cell death. Mice were treated via intragastric administration of atorvastatin for 7 days, injected with KA, and then sacrificed after 24 h. We observed that atorvastatin pretreatment reduced KA-induced seizure activity, hippocampal cell death, and neuroinflammation. Atorvastatin pretreatment also inhibited KA-induced lipocalin-2 expression in the hippocampus and attenuated KA-induced hippocampal cyclooxygenase-2 expression and glial activation. Moreover, AKT phosphorylation in KA-treated hippocampus was inhibited by atorvastatin pretreatment. These findings suggest that atorvastatin pretreatment may protect hippocampal neurons during seizures by controlling lipocalin-2-associated neuroinflammation.